Moreover, in colon cancer cells, tumor necrosis factor α (TNF-α), a proinflammatory cytokine that plays a pivotal role in IBD, was shown to upregulate the de novo pathway of sphingolipid biosynthesis [25], and it is conceivable that this effect could contribute to Cer and SM accumulation in IBD. The gene discussed is TNF; the disease is inflammatory bowel disease.