Due to its ability to evoke spontaneous hypercholesteraemia and arterial lesions resembling those of human atherosclerosis as well as its propensity to be induced to a full spectrum non-alcoholic steatohepatitis (NASH), an ApoE knock-out (ApoE−/−) mouse model is widely used for studying the underlying mechanisms involved in cardiometabolic disease development5–7. Here, APOE is linked to metabolic dysfunction-associated steatohepatitis.