The principal findings include the following: (1) In vivo, during liver fibrogenesis, progerin abnormally accumulates in the nucleus of LSECs, with the loss of SIRT1 and Cav-1, whereas overexpressing SIRT1 with the adenovirus vector can reduce progerin and rescue Cav-1 degradation to attenuate LSEC defenestration and the first stage of liver fibrosis. The gene discussed is CAV1; the disease is Hepatic fibrosis.