Instead, only adipose- and chorionic-derived MSCs reduced AKT and MMP-2 activation, whereas adipose MSCs increased Cav-1 levels; finally, only adipose-derived MSCs attenuated dysregulation of miR-29 and miR-199 [157]. However, in the translation of pre-clinical results to humans, concern remains about the possibility of MSCs to promote fibrosis in the context of the pro-fibrotic microenvironment of IPF. The gene discussed is AKT1; the disease is idiopathic interstitial pneumonia.