Consistently, in a different mouse model of lung fibrosis (hypochlorite-induced) treated with mouse bone marrow-derived MSC[40], amelioration of fibrosis at day 21 was associated with downregulation of the IL6-IL10-TGFβ axis, further corroborating the hypothesis of a critical involvement of M2 macrophages in lung fibrosis, and the ability of MSC in downregulating those inflammatory stimuli leading to persistent M2 activation and expansion. This evidence concerns the gene TGFB1 and pulmonary fibrosis.