Further exacerbating conditions for immune evasion and ectopic proliferation are NK cell death via the Fas–FasL mechanism in early endometriosis, decreased NK cell cytotoxicity, and increased NK cell-mediated cytokine release of TNF-α and IFN-γ, a state which promotes inflammation and angiogenesis required for ectopic endometrial cell lesion survival. This evidence concerns the gene FAS and endometriosis.