On its dimeric form, eNOS-induced NO production fine tunes vascular tone [21,22], in a way to prevent endothelial dysfunction, while actions ending on eNOS configuration to its monomeric state, including the uncoupling from Hsp90 [23] and/or ILK [3,8], prevent eNOS-mediated production of NO, and contribute to the synthesis of superoxide and peroxynitrite radicals [24]. The gene discussed is ILK; the disease is endothelial dysfunction.