Chen and colleagues indicated that the AD-MSCs-mediated anti-pulmonary fibrosis effect involved the anti-inflammatory and anti-apoptosis activities, which are promoted by reducing the pulmonary inflammatory response (downregulation of TNF-α, IL-1β, IL-6, and IL-10) and inhibition of mitochondrial apoptosis-related protein (Caspase-3) expression. Here, IL6 is linked to pulmonary fibrosis.