The Toll-like receptor 4 (TLR4)-myeloid differentiation primary response 88 (MyD88)-nuclear factor κB (NF-κB) pathway is stimulated by excessive levels of saturated fatty acids (SFA) in NAFLD, leading to increased expression of downstream inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β and thereby contributing to the pathogenesis of NAFLD [76]. Here, TLR4 is linked to metabolic dysfunction-associated steatotic liver disease.