To overcome these limitations, ASO or siRNA targeting STAT3 (a key regulator of inflammation) was loaded into BMSC-EVs, and the engineered iExosiRNA-STAT3 or iExomASO-STAT3 treatment showed higher potential to reduce collagen I deposition and α-SMA, vimentin and FN expression in a CCl4-induced liver fibrosis model (149). The gene discussed is ACTA1; the disease is Hepatic fibrosis.