The former disrupts the stability of the MHC-I complex, leading to loss of MHC-I expression on tumor cells and preventing T cell-mediated recognition and killing, with B2M mutations or deletions being a key example [123, 124], while JAK1/JAK2 loss-of-function mutations impair IFN-γ responsiveness, reducing PD-L1 and MHC-I induction [125–127]. Here, CD274 is linked to neoplasm.