CD36 and pulmonary fibrosis: A study revealed a decrease in cluster of differentiation 36 (CD36), a protein involved in fatty acid transport and PPAR signaling, in both human and murine dermal fibrosis, further supporting the association between FAO and extracellular matrix regulation.[13] Consistent with this research, our study demonstrated that pioglitazone, an activator of FAO, promoted the resolution of silica‐induced lung fibrosis by facilitating ECM internalization by myofibroblasts.