A recent study showed that CPT1A and CPT2 were crucial for the glycerol phospholipid remodeling [27], and cigarette smoking-induced mtROS inhibited the expression of PPARα and CPT1A in lung fibrosis [42], which are in line with previous studies demonstrating that PPARα activators exerted anti-fibrotic effects in the lung [45] and another organ such as liver and kidney [42]. This evidence concerns the gene CPT1A and pulmonary fibrosis.