Huang S. et al. (2022) reported that ASPN could promote lung myofibroblast differentiation by facilitating TGF-β/Smad signaling. Huang C. et al. (2022) unveiled that ASPN could attenuate fibrosis in cardiac remodeling by regulating mitochondrial bioenergetics and protecting cardiomyocytes from hypoxia–reoxygenation-mediated cell death. Liu et al. (2021) showed that ASPN participated in keloid progression by disturbing interfibroblast mechanocommunication and inhibiting matrix remodeling. The gene discussed is TGFB1; the disease is keloid.