However, these results by no means preclude that bacterial endotoxin may also activate IL1β and IL6 as well as iNOS through TNFα-independent pathways; rather, our results suggest that in the early phase of MASLD, TNFα may be one of the key mediators in the development of diet-induced non-obese MASLD. The gene discussed is IL6; the disease is metabolic dysfunction-associated steatotic liver disease.