Steve: And when it comes to other strategies, senescence, right now it's a hot topic, the so-called senolytics that remove senescent cells, you know. And we are about to analyze data collected by James Clement who did clinical trials of these senolytic strategies, and hopefully, we'll have an answer in a couple of weeks, you know, but I just don't know whether removing senescent cells has an effect on epigenetic age.

In general, the relationship between senescence and epigenetic age is complicated because when it comes to inducing senescence, there's several ways of inducing senescence. One is simply what is known as replicative senescence, you passage cells, you split them and let them grow, and grow, and grow. And that form of senescence is somewhat related to epigenetic clocks. Then there are other forms, so-called radiation-induced senescence, you radiate the cell. And that form of senescence doesn't seem to accelerate the epigenetic clocks, you know. So, it's complicated. And conversely, there are ways of immortalizing cells by over-expressing the component of the telomerase, the TERT. So, immortalizing a cell actually it doesn't stop epigenetic aging. You can even immortalize cells that you can passage for decades, but the epigenetic age keeps going up in those cells.

Rhonda: Really?

Steve: Yes. So, do you see? Epigenetic clocks are not simply markers of cellular senescence. They really pick up a different aspect of biology.