More broadly, it is known that KRAS hyperactivation can influence the immune tumor microenvironment through various mechanisms, including direct secretion of immune suppressive cytokines by tumor cells [32], recruitment and activation of T regulatory cells [33], PD-L1 hyperexpression [34], sensitization of cytotoxic T cells to activation-induced cell death [35], and suppression of interferon signaling [36,37]. Here, CD274 is linked to neoplasm.