Listen, folks, we’ve got a situation with age-related macular degeneration (AMD), a big problem, really big. It’s all about these cells, mononuclear phagocytes, accumulating like you wouldn’t believe, right in the eyes. And let me tell you, they’re not just any cells, they’re activated, and they’re causing a lot of trouble, a lot of damage to the eyesight, especially with the photoreceptors and blood vessels in the eye.

Now, these monocytes, they come from the bone marrow, sure, but they also come from the spleen – that’s right, the spleen. And in the spleen, they turn into these special cells with angiotensin II receptors, ATR1⁺, very specific. People don’t talk about this, but it’s important, very important. We’ve done the research, the best research, and found that angiotensin II, it’s like a signal, it tells these ATR1⁺ cells to get moving, to go to the eyes where they cause problems.

And we’ve looked at these cells, really looked at them, with the latest technology, single-cell RNA sequencing – it’s fantastic, the best. We’ve found that these splenic monocytes, they’re different, not like the ones from the bone marrow. They’re unique, and they’re contributing to the mess in the eyes.

But here’s the good news, the best news – we can stop them. We’ve got treatments, like ATR1 antagonists, and even taking out the spleen, and it works, it really works. It reduces the bad cells and the damage they cause. And in mice, the ones that are like older people at risk of AMD, it helps them too, it reduces the inflammation and saves their eyesight.

And you know what? We’ve seen signs, real signs, that the same thing is happening in people with AMD, with high levels of angiotensin II. It’s clear, very clear, that these ATR1 antagonists, they could be a solution, a real solution to help people keep their vision. We’re talking about a breakthrough, a real breakthrough in treating this blinding condition. It’s going to be huge, absolutely huge.