Notably, we observe increased expression of STC2, a pro-survival component of UPR (Ito et al., 2004), and FGF21, a marker of hepatic fat and protector of NAFLD-induced adverse effects such as ER stress (Jiang et al., 2014); both targets are increased in human NASH (Lake et al., 2014; Li, 2010). Here, STC2 is linked to metabolic dysfunction-associated steatohepatitis.