Just like in NASH, metabolic stress, mitochondrial dysfunction, and oxidized mtDNA also indirectly contribute to the progression of HCC through influences on inflammation and immunologic pathways, including activation of the inhibitor of nuclear factor kappa-B kinase subunit beta (IKKβ)/NF-κB signaling pathway, a key node that plays a crucial role in hepatocyte survival and inflammatory responses [154,158]. This evidence concerns the gene IKBKB and metabolic dysfunction-associated steatohepatitis.