Yesterday I explained the paradox sitting at the center of the artificial intelligence (“AI”) boom.

America is building a new railroad – hundreds of billions of dollars a year poured into data centers. And like every railroad before it, it will destroy as much as it creates. As the cost of computing falls toward zero, every business model that depends on charging for computing stops working.

So the question for investors is not what AI will build. The most important question investors must answer today is: what industry that uses massive amounts of compute will AI not destroy?

Biotechnology. It is the only industry that can absorb unlimited computing power and still defend its prices, because the government hands a drug company a legal monopoly. The moat is the government.

So… the next question is… which new drugs will generate the greatest revenue? I told you yesterday, it’s drugs that deal effectively with obesity. But… heart disease is not far behind.

You probably think heart disease is a solved problem because you know about cholesterol. You know your doctor checks it. You know that if the number is high he puts you on a statin, and that statins work – they are one of the genuine triumphs of modern medicine, and they have saved millions of lives, probably including someone you love.

But there’s a lot more to this problem that isn’t solved – yet.

There might be a second kind of cholesterol particle in your blood. Your doctor has almost certainly never measured it. Over the entire decade from 2015 through 2024, fewer than 730,000 Americans were ever tested for it. It is called lipoprotein(a) – or Lp(a).

Picture an ordinary cholesterol particle. Now wrap a second, tangled protein around the outside of it – a protein that makes the particle sticky, inflammatory, and prone to helping blood clot. That is Lp(a). It does not merely clog the artery. It irritates the artery wall and then makes the clot that finishes the job.

And here is the part that ought to alarm you. Why does the disciplined 52-year-old – lean, active, statin-compliant, textbook numbers – drop dead in the driveway? Lp(a).

What can you do about it? Nothing.

Your Lp(a) level was set the day you were conceived. It is written in your genes. It does not move.

Diet does not lower it. Exercise does not lower it. Losing 40 pounds does not lower it. Statins do not lower it. You can do everything your doctor tells you, achieve perfect cholesterol numbers, run a marathon at 50 – and your Lp(a) will not change.

About one person in five carries a dangerous level of Lp(a) – that’s 65 million Americans and 1.5 billion people worldwide.

The risk is not subtle. If your Lp(a) is above 180, your danger of a heart attack is in the highest risk category. If you have already survived one heart attack and your level is above 100, you are more than twice as likely to have another – and if you are under 60, more than three times as likely. Among patients already taking a statin, with their cholesterol driven down to target level, high Lp(a) leaves 38% excess risk sitting there untouched.

For 60 years, doctors could measure Lp(a) and do nothing about it. There is still not one approved drug that lowers it. The only treatment that exists is to run the patient’s blood through a filtration machine on a repeating schedule, at a cost of $50,000 to $150,000 a year.

So why has no one drugged it?

Because you cannot get at Lp(a) the way medicine normally works. Almost every drug you have ever taken is a blocker. It finds a finished protein doing damage and jams it. But Lp(a) is not a lock you can pick. To stop it you have to prevent the liver from building it in the first place – which means reaching inside the cell and destroying the instruction before the protein exists!

And that’s our Fourth (of my 11) Kingdom of Medicine: gene silencing.

Think of your DNA as the master blueprint locked in a vault. The cell never sends the blueprint to the factory floor. It sends a working copy – a paper work order called messenger RNA. The factory reads the work order and builds the protein.

Conventional drugs wait at the end of the line and smash the finished product. Gene silencing walks over to the factory floor and shreds the work order. No work order, no protein. And because one shredder handles thousands of copies, a single injection can keep a gene switched off for months.

Two American scientists, Andrew Fire and Craig Mello, discovered this mechanism in a worm in 1998. And finding that worm won the Nobel Prize for them eight years later. Gene silencing will become the biggest innovation in medicine since the invention of monoclonal antibodies. And this technology’s first great triumph will be Lp(a).

There are four companies in the final stretch, waiting for results from pivotal Phase III trials. The leader cuts Lp(a) by about 80% with a monthly injection. It’s enrolled 8,323 patients with established heart disease. When the study is complete, it will be the first to prove conclusively that lowering Lp(a) prevents heart attacks. The trial is expected to end later this year.

No, this will not be a one-drug only field. There are three other similar gene-silencing drugs in development. But, critically, none of them will finish their own pivotal trials until 2028 or beyond. And that means… the drug that’s first to market will have a huge advantage.

And there’s more.