Cynthia Lebeaupin and colleagues found that BI-1 gene ablation in tunicamycin-treated BI-1−/− mice made the liver vulnerable to NAFLD, which led to hepatic steatosis and metabolic collapse; this was evidenced by an increase in fatty acid uptake, inhibition of β-oxidation, and a reduction in fatty acid release. The gene discussed is TMBIM6; the disease is metabolic dysfunction-associated steatotic liver disease.