Thus, from the point of view of downstream mechanisms in the STAT5 hypothesis, we investigated (a) whether SMC-specific deletion of STAT5a/b in the mouse had an effect on expression of BCL6 in SMCs in pulmonary arterial tunica media and (b) whether SMC-specific deletion of BCL6 in the mouse had an effect on chronic hypoxia-induced PAH and its male-dominant sex-bias phenotype (Figure 1). Here, BCL6 is linked to pulmonary arterial hypertension.