Oxidative stress has been recognised amongst the contributing factors in the progression of steatosis [2,17] with involvement of nuclear factor-κΒ (NF-κΒ) activation and increased release of proinflammatory cytokines, such as tumour necrosis factor alpha (TNFα) and the interleukin-6 (IL-6) representing the second insult in the “two hits” model [18,19]. This evidence concerns the gene TNF and steatosis.