2013; Krokowski et al. 2013). Thus, it has been proposed that inhibiting protein synthesis may be a therapeutic strategy for treating ER stress‐related diseases (Han et al. 2013). In support of this concept, we recently showed that decreasing protein synthesis with an inhibitor of eukaryotic elongation factor 1A (EEF1A), didemnin B, protected HepG2 cells from death induced by exposure to high palmitate (Stoianov et al. 2015), an in vitro model of the hepatocyte lipotoxicity that occurs during NAFLD progression. The gene discussed is EEF1A1; the disease is metabolic dysfunction-associated steatotic liver disease.