Taken together, our results add further weight to the hypothesis that an increased translocation of bacterial endotoxin may through TNFα- and JNK-dependent signaling cascades enhance the formation of cytokines like IL1β and IL6 and of pro-oxidative mediators like NO2− thereby adding to the onset and probably also progression of MASLD. The gene discussed is IL1B; the disease is metabolic dysfunction-associated steatotic liver disease.