Fumonisin B, a mycotoxin produced by Fusarium moniliforme, causes neuronal degeneration, liver and renal toxicity, cancer, and another injury to animals. It was discovered, that fumonisin B1 inhibited sphingosine (sphinganine) N-acyltransferase and de novo sphingolipid biosynthesis. It was suggested, that fumonisin B1 might have two modes of interaction with ceramide synthase. The “sphinganine-like” domain may interact with the sphinganine binding site, and the negatively charged tricarbyllic acid groups may interact with the fatty acyl-CoA binding site (by mimicking the polyanionic phosphate groups of the CoA). The latter interaction is probably not the most important because fumonisin B1 does not inhibit another CoA-dependent enzyme (serine palmitoyltransferase) or labeling of glycerolipids. The ability of fumonisin B1 to interact with both binding sites might account for its potency.