Suppose PDL1 (like LAG3) is not only a CPI but also a stemness marker (unlike other CPI), could that explain why anti-PD1/L1 (and anti-LAG3) is a better anti-cancer treatment compared with those other CPI (e.g., anti-CTLA4, anti-IDO1, anti-TIGIT), which are bona fide immunotherapy? The gene discussed is LAG3; the disease is cancer.