We observed that SMC-specific heterozygous or homozygous deletion of STAT5a/b abrogated the male-dominant sex bias in that both female and male mice developed PAH (increased right ventricular systolic pressure (RVSP), hypertrophy of pulmonary arterial vessel wall, and right ventricular hypertrophy) to a similar extent [19–21]. This evidence concerns the gene STAT5A and pulmonary arterial hypertension.