Mechanistically, triggering of human hepatic in vitro models resulted in the activation of NASH-specific upstream regulators, including soluble inflammatory mediators and TLRs, as well as transcription factors and kinases known to be activated in the livers of NASH patients, such as NFκB, Jun, and p38 MAPK [23,24]. Here, JUN is linked to metabolic dysfunction-associated steatohepatitis.