Cisneros et al. [5] reported a correlation between HSC activation and rate of fibrosis progression in patients with recurrent HCV post-transplant; however, they did not show any difference in HSCs activation and accelerated fibrosis as compared to non-LT patients with chronic hepatitis C. Venturi et al. [42] reported that ≥ 8% activated HSCs (α-SMA%) at 6-month post-transplant in paediatric patients is an independent risk factor for 7-year fibrosis development and that α-SMA% ≥ 8% at 3-year post-transplant is associated with fibrosis development at 7 years. The gene discussed is ACTA1; the disease is chronic hepatitis C virus infection.