BCL3 and congenital bilateral aplasia of vas deferens from CFTR mutation: Notably upregulated genes include CYP1B1, a cytochrome P450 family enzyme shown to be atheroprotective (28, 29) and associated with decreased oxidative stress and inflammation (30); BCL3, an NFκB inhibitor associated with atherosclerotic changes (31); IL6R, the interleukin-6 receptor, mutations of which have been implicated in increased vulnerability to CAVD (32, 33); and NQO1, an NAD(P)H oxidoreductase for which upregulation has been linked with decreased calcification (34).