The apparent contribution of the NDPK-B/Gβγ- and the NDPK-B/SK4-interaction to HF and atherosclerosis, respectively, give raise to the assumption that interference with the histidine kinase activity of NDPK or even more specifically, the inhibition of the interaction of the NDPK-B with its target proteins by small molecule inhibitors might offer avenues for future treatments of cardiovascular diseases. The gene discussed is CFB; the disease is hydrops fetalis.