Here's an explanation of how anti-PD-1 drugs work. It's probably TMI.

PD-1 is a protein found on the surface of immune cells (not cancer cells). When the immune cell is in position to kill a target cell, PD-1 can bind to a protein on the surface of the target cell called PD-L1 and this prevents the killing. So expressing PD-L1 is one way that cancer cells escape killing by the immune system. Keytruda, Jemperli, and several similar drugs prevent the PD-1 to PD-L1 interaction and restore killing of cancer cells by immune cells.

But there's something else needed for the immune system to want to kill the cancer cells in the first place. It has to recognize the cancer cells as abnormal. The main way this happens is because the cancer has mutations, some of which cause it to make abnormal proteins. The immune system can detect these abnormal proteins.

Some cancers have thousands of mutations and so make thousands of abnormal proteins that can generate an immune response. Other cancers only have a few mutations. So using Keytruda etc. to unleash the immune system works much, much better on cancers with lots of mutations. Cancers that are defective in the DNA repair process called mismatch repair (MMR) have lots of mutations. So do cancers with mutations in the gene POLE, as well as melanomas (which have uv-induced mutations) and lung cancers, particularly in smokers. So Keytruda etc can have dramatic effects on these cancers.

Endometrial cancers that are proficient in MMR (pMMR) tend not to have many mutations, so there's not a high likelihood of a major response to Keytruda or Jemperli. They do give them to people anyway, since there is a modest improvement in prognosis with them.