Our hypothesis that TBE-31 protects against excessive hepatic steatosis, at least in part, by blunting ER stress, could be likened to protection against the toxic effect of the ER stressor tunicamycin by the Nrf2 activator 3H-1,2-dithiole-3-thione,51 or protection conferred by knockdown of Keap1 against the ER stress-mediated apoptotic effects of alkylating agents.52 The gene discussed is KEAP1; the disease is Hepatic steatosis.