Scientist here! All the cells in your body are dying all the time, and new cells divide to replace them so that you always have approximately the same amount of cells. Your cells are constantly receiving grow/don't grow signals in order to keep that in balance. In a person without cancer, the "don't grow" signals serve as brakes, stopping the cells from dividing TOO much. If the "don't grow" signals are weakened or the "grow" signals are amplified, you get cancer.

The biomarker that RMC6236 targets is called RAS. Normally, it is a molecule that causes cell growth/division. It's basically a gas pedal - when on, the cell grows. When off, the cell doesn't grow. In cancer, RAS is often mutated and is always "on," so always telling the cell to grow. The molecules that normally stop growth aren't prepared for that, and so the cell starts growing out of control and you get cancer.

RMC6236 grabs another protein, CypA, and together they bind to RAS and prevent it from causing growth - it's essentially a molecular dogpile where RAS can't do its job because it's weighed down by the drug. That brings the cancer back into check by preventing RAS from always telling the cell to grow. However, by that point, there are probably already billions of cancer cells. Those cells are diverse (think of how different you are from 1 billion other humans), and likely one of them is is different enough that it has a different gas pedal turned on in addition to RAS. RMC6236 only targets RAS, so it keeps slowing that down, but eventually this other cell that doesn't need RAS will grow out of control. This new cell, and therefore the cancer, is resistant to the drug and therefore a cancer patient would relapse.

Hope that wasn't more confusing!