2009; Olson et al. 2012; Ash et al. 2013a). In support of this premise are our final multivariable regression models that showed resting AASI and endothelin‐1‐21 levels were positively correlated with the magnitude of PEH, suggesting that VIGOROUS overrode the greater vasoconstrictive nature of the vasculature of AF at rest via increased NOS3 expression and NO production and availability, as well as by other peripheral and central mechanisms we did not measure. The gene discussed is NOS3; the disease is atrial fibrillation.