Increases in oxidative stress and in factors that promote proinflammatory cytokine expression, such as interleukin (IL)-6 [13] and tumor necrosis factor-α (TNFα) [14], are implicated in the development of nonalcoholic steatohepatitis (NASH), with the nuclear factor kappa B (NF-κB) playing a critical role in the modulation of proinflammatory transcription [15]. Here, TNF is linked to metabolic dysfunction-associated steatohepatitis.