The increased EPCs had been shown as a reflection of a functional bone marrow response to diffuse and severe endothelial damage during the early stages of HF, but an additional and significant increase of tumor necrosis factor (TNF-α) counteracted and overwhelmed the elevation of EPC mobilization in advanced disease phases by exerting a possible suppressive effect on hemopoiesis [59]. The gene discussed is TNF; the disease is hydrops fetalis.