Findings on the source of cytoplasmic [Ca2+], the participation of caldesmon in the regulation of contraction, alterations in RhoA/ROCK sensitivity and the non-involvement of cofilin and LIM kinase (LIMK) in PAH smooth muscle contraction open new avenues to modulation of the excessive contraction taking place in pulmonary arterial hypertension. This evidence concerns the gene CALD1 and pulmonary arterial hypertension.