The altered circulating milieu of cytokines in MASLD induces a state of low-grade chronic inflammation, enhances the nuclear transcription factor kappaβ (NF-κβ) signaling, and triggers a cascade of pro-inflammatory mediators such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1 β (IL-1β). This evidence concerns the gene TNF and metabolic dysfunction-associated steatotic liver disease.