These findings open new arenas that are critically relevant to the clinicians in providing better prognostic and diagnostic tools, by identifying BiP or other ER stress molecules along the signaling pathway, as therapeutic targets and adopting measures that alleviate apoptotic responses, prevent or slow down the pathogenic progression of reversible NAFLD to irreversible NASH in patients with FH. The gene discussed is HSPA5; the disease is familial hyperaldosteronism.