Importantly, pulmonary hypertension [45], angiotensin II-triggered cardiac remodeling [46], and diabetic cardiomyopathy [47] were all shown to be relieved by PKM2 activation, either by genetic modification or pharmacological manipulation, through multiple mechanisms such as inhibition of TGF-β/Smad2/3 and Jak2/Stat3 pathways, oxidative stress, and NLRP3 inflammasome. Here, JAK2 is linked to pulmonary hypertension.