As a matter of fact, elevated RV titin-based stiffness was reported in human patients with primary pulmonary arterial hypertension as well [63], but its mechanism seems to be different than that of the post-ischemic failing heart in our study, since only PKA could lower RV cardiomyocyte stiffness, but neither CaMKIIδ nor PKCα incubation had significant mechanical effect in those experiments [64]. The gene discussed is PRKCA; the disease is idiopathic pulmonary arterial hypertension.