This discovery focused our attention on the possibility that the resolution of the species-specific sex-bias paradox in PAH between human females (greater susceptibility to PAH than males) and rodent females (lesser susceptibility to PAH than males) might reside in the well-known differences in the patterns of sex-biased secretion of growth hormone (GH)—a well-characterized upstream activator of STAT5a/b [19–21]. The gene discussed is GH1; the disease is pulmonary arterial hypertension.