Glucose control might impact MASLD by favouring the accumulation of triglycerides within the hepatocytes through the activation and upregulation by hyperglycaemia of key transcriptional factors involved in de novo lipogenesis, such as carbohydrate responsive element binding protein and sterol regulatory element binding protein-1c [11, 12]; furthermore, in animal models, hyperglycaemic conditions over-express glucose transporter 2 that may contribute to liver fat accumulation by an overflow of glucose in the hepatocyte [26]. Here, MLXIPL is linked to Hyperglycemia.