Upon injury, lung resident MSCs get activated and are differentiated into myofibroblasts, leading to increased α-SMA expression and collagen secretion, thereby causing diseases such as pulmonary fibrosis and bronchiolitis obliterans (popcorn lung).15 Chronic inflammation upregulates the pro-inflammatory factors (eg, TNF-α and IL-6) and pro-fibrotic factors (eg, TGF-β) in the idiopathic pulmonary fibrosis initial stages.15 TNF-α-initiated NF-κB signaling induces the differentiation of LR-MSCs to myofibroblasts and leads to lung fibrosis. This evidence concerns the gene ACTA1 and pulmonary fibrosis.