Dual inhibition of TLRs in macrophages, known to drive inflammatory responses to DAMPs and PAMPs, and TGF-β signaling in fibroblasts and myofibroblasts that drive fibrotic responses, may allow us to target a number of human diseases in which these signaling pathways are upregulated to enhance inflammation associated fibrotic scarring, including NASH, idiopathic pulmonary fibrosis, kidney disorders, cystic fibrosis, and adipose tissue fibrosis in obesity, among others. This evidence concerns the gene TGFB1 and metabolic dysfunction-associated steatohepatitis.