MET augmented both immunogenicity and recognition of tumor cells; downregulated Kras (oncogene), Bcl2, and Bclxl (anti-apoptotic proteins); blocked the synthesis of inflammatory cytokines; reduced immune checkpoints (2b4, Flgl1, Lag3, Pd-11, Pd-1) in tumor cells, and increased CD4+T, CD8+T, and macrophages (M1) infiltration [164]. The gene discussed is BCL2; the disease is neoplasm.