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Thank you for verifying. Point 2) is an interesting one because I had a theory before Munich that cancer cells have evolved an evolutionary tactic to not express PDL one allowing them to hide from the immune system and inappropriate response to kill the cancer cells.

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That's not how it works. When PD-L1 is expressed active T-cells ignore the tumor because PD-L1 sends out a do not kill signal. PD-L1 would have developed evolutionarily to keep an out of control immune system from killing healthy cells. The genetic aberrations that lead to cancerous tumors are often also accompanied by genetic aberrations that make those tumors preferentially express PD-L1 when confronted with active T-cells. The lack of PD-L1 doesn't stop the tumor from being recognized by the immune system. It's an active immune system that will attack the tumor that increases PD-L1 in response.

Tumors can lower HLA-DR, which I mentioned in a previous post, to escape detection. An M2 macrophage tumor microenvironment dominated by Tregs will cause the immune system to ignore tumors. Leronlimab reverses both.