As we previously showed that Rad51b knockout decreased luciferase signaling and ERα expression during tumor progression, combination treatment with low-dose EZH2i (20 mg/kg) efficiently blocked the effects caused by RAD51B deficiency (Fig. 6l–K and S7D), indicating that inhibiting the EZH2 pathway can effectively maintain ERα-mediated signals even when tumors lose RAD51B expression. The gene discussed is EZH2; the disease is neoplasm.