Intriguingly, it has been reported that the treatment of human endothelial cells with iTFAs promotes NF-κB activation and subsequent induction of pro-inflammatory cytokines,17 and that iTFA administration to peroxisome proliferator-activated receptor α (PPARα)-deficient mice exacerbates metabolic dysfunction-associated steatotic liver disease (MASLD)/metabolic dysfunction-associated steatohepatitis (MASH) with increased NF-κB activation and inflammation.18 The gene discussed is NFKB1; the disease is metabolic dysfunction-associated steatohepatitis.