All endometriosis forms share certain immunopathogenetic mechanisms: peritoneal macrophage accumulation and their polarization toward regenerative phenotype, reduced NK cell cytotoxicity, elevated local proinflammatory cytokine levels (IL-1β, IL-6, IL-8, TNF-α) with simultaneous increases in immunosuppressive mediators (IL-10, TGF-β), collectively creating favorable conditions for ectopic tissue development. The gene discussed is IL1B; the disease is endometriosis.