IFNG and neoplasm: Most of these ultimately are driven by any number of developments: tumor mutations and adaptations, reduced neoantigen generation or expression, disfunction of MHCs, resistance to IFN-γ signaling, indoleamine 2,3-dioxygenase (IDO) overexpression, loss of phosphatase and tensin homologue (PTEN) expression, and overexpression of the Wnt–β-catenin pathway and so on [75, 76].