The antitumor mechanism of CAR–MAIT cells exhibits triple synergy: (1) CAR‐dependent pathway—recognizing tumor surface antigens through the CAR; (2) TCR‐dependent pathway—recognizing 5‐OP‐RU presented by MR1 on the surface of tumor cells or APCs (some tumor cells can upregulate MR1 expression under stimulation by microbial metabolites); (3) NK‐like pathway—recognizing stress ligands (e.g., MIC‐A/B) via NK‐activating receptors (such as NKG2D and DNAM‐1). This evidence concerns the gene MR1 and neoplasm.