As PGC-1α is well-established to mediate mitochondrial biogenesis and metabolic stress adaptation in other cell types6, we examined PGC-1α expression in endothelial cells from wild-type (WT) mice treated with a pressor dose (i.e, a dose known to induce endothelial dysfunction in WT mice) of angiotensin II (ATII). The gene discussed is AGT; the disease is endothelial dysfunction.