Under competitive interaction with CD226 and CD96 for binding to CD155, TIGIT may disrupt CD226 co‐stimulation and produce inhibitory signals leading to suppression of antitumor immune responses.13 A recent study indicated that TIGIT predominantly regulates immune responses through CD4+ Tregs,14 whereas CD4+ Tregs abundance was correlated with tumor burden in OC patients.15 Therefore, we hypothesized that TIGIT‐mediated immune suppression through enhancing CD4+ Tregs responses during OC. The gene discussed is CD226; the disease is neoplasm.