Stimulation of the LPS-TLR4 signaling pathway induces the interaction of TLR4 with the adaptor molecule MyD88 and eventually leads to the release of proinflammatory mediators such as TNF-α [36], which ultimately causes inflammation and progression of MAFLD to NASH and subsequent fibrosis [37,38]. Here, TNF is linked to metabolic dysfunction-associated steatohepatitis.