Emerging research delineates that inhalation of carbon monoxide at a low concentration (250 ppm) can mitigate ritonavir-induced myocardial fibrosis through modulation of both canonical (Smad2-mediated) and non-canonical (p38 MAP kinase-mediated) TGF-β1 signaling pathways [64]. Here, TGFB1 is linked to Myocardial fibrosis.