KRAS and neoplasm: This MHC-dependent mechanism enables TCR-T cells to recognize intracellular tumor-associated or tumor-specific antigens that are processed and presented via MHC molecules, such as cancer/testis antigens (e.g., NY-ESO-1 and MAGE-A4) and neoantigens derived from somatic mutations (e.g., KRAS G12D) [11].