During the development of NAFLD, FFA governing transcription regulators are disrupted (e.g. the transcription factors peroxisome proliferator‐activated receptor alpha [PPARα], or sterol regulatory element‐binding proteins [SREBPs]) causing inappropriate activation of pro‐inflammatory signalling pathways (via protein‐kinase B [AKT] or AMP‐activated protein kinase [AMPK]) that contribute to the production of pro‐inflammatory cytokines such as IL‐6, TNF‐α or IL‐1β and increased hepatocellular damage.8, 29. Here, AKT1 is linked to metabolic dysfunction-associated steatotic liver disease.