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. This evidence concerns the gene PPARA and pulmonary fibrosis.