For example, inhibition of glycolysis blunted the differentiation of lung fibroblasts into myofibroblasts and attenuated profibrotic phenotypes in myofibroblasts isolated from the lungs of patients with idiopathic pulmonary fibrosis [31].The contribution of HIF-1a pathway in the metabolic switch observed in DMD hiPSC-derived cardiac fibroblasts was not examined in the present study and needs to be further explored as over-expression of hypoxia-inducible factor 1-α, was shown to potentiate myofibroblast differentiation [32]. This evidence concerns the gene HIF1A and pulmonary fibrosis.