This pathway is regulated by multilevel processes, with tumor cell energy metabolism activating ATP-activated protein kinase [66,67], leading to the upregulation of the BTN2A1–BTN3A1–BTN3A2 complex and the enhanced binding of PAg, thereby enabling Vγ9Vδ2 T cells to recognize and exhibit cytotoxicity toward tumor cells [68]. The gene discussed is BTN2A1; the disease is neoplasm.