(180) discovered that patients with KRAS and LKB1-mutated (KL) NSCLC, together with KL murine cancer cell lines and genetically engineered mouse models (GEMMs) of lung cancers, have a low immunoproteasome activity and increased autophagy flux; these features compromise the processing and presentation of antigens to MHC-1, leading to evasion of the immune response by tumor cells. Here, KRAS is linked to neoplasm.