Given that Treg cells exhibit robust expression of the chemokine receptor CCR8, which drives Treg recruitment, as well as TNFRSF4, which functions as a costimulatory molecule (Figure 6D), we proposed the following approaches: employing anti‐CCR8[36] antibodies to mitigate Treg infiltration and stimulating TNFRSF4[37] to counteract Treg‐mediated immunosuppression in HRD tumors. The gene discussed is TNFRSF4; the disease is hypoparathyroidism-retardation-dysmorphism syndrome.