IFNG and neoplasm: In line with this notion, the likelihood of individual patients responding to ICIs (which significantly varies across tumor types) depends on (1) tumor infiltration by immune effector cells at baseline, which most often results in interferon gamma (IFNG)-dependent expression of PD-L1 by malignant and myeloid cells, and (2) tumor mutational burden, which is largely correlated with the ability of neoplastic cells to present antigenic determinants that are not covered by central tolerance and hence can effectively drive adaptive immunity [195].