Given the role of SERCA2a on STAT3 activity [18,19] and the role of STAT3 in PAH as well on BMPR2 expression and downstream targets [16,23,24,25], we tested whether SERCA2a and STAT3 inhibition modulate BMPR2 expression in hPASMCs by using HJC0152 compound, a novel STAT3 inhibitor, and its downstream target genes (c-Myc and Cyclin D1) [26,27,28]. This evidence concerns the gene CCND1 and pulmonary arterial hypertension.