Given the relevance of ERK1/2 in lung fibrosis31 and since PPARγ can serve as a substrate for MAPK28,32, we validated the effect of metformin in inhibiting the activity of ERK1/2 by western blotting and the results showed robust inhibition of p-ERK1/2 levels in IPF lung fibroblasts in response to metformin treatment (Supplementary Fig. 5B). Here, MAPK3 is linked to idiopathic pulmonary fibrosis.