Therefore, targeted inhibition of excessive Fas/RIPK1 pathway activation - by reducing Fas/FADD/Caspase-8/RIPK1-PANoptosome complex assembly, decreasing abnormal “Find-me” signal release, and limiting downstream immune cell recruitment - may serve as a key therapeutic strategy to disrupt the vicious “apoptosis signal-inflammatory feedback” cycle in endometriosis. The gene discussed is RIPK1; the disease is endometriosis.