We and others demonstrated that exposure to a single dose of ionizing radiation (IR) suppresses expression and functioning of TM17 and eNOS18, resulting in endothelial dysfunction, and that administration of recombinant TM19 or treatment with pharmacological inducers of TM and eNOS mitigate the damage caused by single exposure of IR18,20,21. The gene discussed is NOS3; the disease is endothelial dysfunction.