Currently, inhibition of EV secretion, such as GW4869 (nSMase2 inhibitor), tipifarnib (farnesyltransferase inhibitor), and neviramine (Rab27a inhibitor), has demonstrated efficacy in suppressing tumor‐derived EVs release, thereby attenuating immune evasion in preclinical models.[61, 62] Several of these agents are currently under evaluation in early‐phase clinical trials in combination with immunotherapies.[63, 64] The application of high‐affinity neutralizing agents such as anti‐PD‐L1 agents, including atezolizumab and durvalumab, is already widely used in clinical practice. The gene discussed is SMPD3; the disease is neoplasm.