TNFRSF12A and neoplasm: To elucidate the underlying molecular mechanisms, cellular experiments revealed that TNFRSF12A knockdown resulted in (1) significantly compromised angiogenic capacity in HUVEC tube formation assays (p < 0.01); (2) markedly augmented cytotoxicity of T cells against tumor cells (p < 0.05); and (3) reduced cellular sensitivity to docetaxel, as evidenced by significantly elevated IC50 values in CCK-8 assays (p < 0.01).