Therefore, it can be justifiably predicted that Lcn2 might be a key inducer of oxidative stress following HMGB1 secretion in brain under NASH physiology via its interaction with either TLR4/RAGE pathway and that might involve NOX-2, a key generator of highly reactive superoxide radicals and hydrogen peroxide. Here, LCN2 is linked to metabolic dysfunction-associated steatohepatitis.