Also, ER stress was evidenced to contribute to HSC activation; the possible regulatory mechanism was that ER stress in HSCs could promote liver fibrosis by inducing overexpression of SMAD2, via dysregulation of miR18a, and this dysregulation was mediated by PERK phosphorylation and destabilization of HNRNPA1 (Koo et al., 2016). The gene discussed is SMAD2; the disease is Hepatic fibrosis.