GLS and pulmonary arterial hypertension: GLS1 inhibitor (CB‐839) was effective in reducing vascular collagen content, vascular stiffness, and proliferation, as well as histologic and hemodynamic parameters of pulmonary hypertension.[37] Furthermore, BPTES partially prevented aortic valve thickness, fibrosis, and calcification.[13] Inhibition of glutaminolysis (CB‐839) in activated myofibroblasts, protects against cardiac functional decline and fibrosis.[12] GLS1‐related glutaminolysis aggravates age‐associated disorder.