The resulting chimeric structure (mim γ-BiPPB) could solely bind to the PDGFβR on activated HSCs and considerably blocked CCl4-induced acute and chronic stages of hepatic fibrosis in mice as indicated by a reduction of α-SMA, desmin, and collagen type I mRNA and protein expression, while off-target effects were not observed (Bansal et al., 2014b). The gene discussed is ACTA1; the disease is Hepatic fibrosis.