EPO can reduce cytokine gene expression in endothelial cells exposed to tumor necrosis factor [204], prevent ulcer progression in cases of scleroderma [205], modulate inflammation during experimental autoimmune encephalomyelitis [206], reduce inflammation in murine arthritis models [207], and block primary microglial activation and proliferation during oxidative stress [25,78] to prevent phagocytosis of injured cells through pathways that involve cellular membrane PS exposure, protein kinase B (Akt) [49], and the regulation of caspases [78,208,209]. This evidence concerns the gene AKT1 and arthritic joint disease.