The first step in the biosynthesis of sphingolipids is the condensation of serine and palmitoyl CoA, a reaction catalyzed by serine palmitoyltransferase (SPT) to produce 3-ketodihydrosphingosine (KDS). Although SPT is a housekeeping enzyme, its activity is regulated transcriptionally and post-transcriptionally, and its up-regulation is suggested to play a role in apoptosis induced by certain types of stress. Specific missense mutations in the human LCB1 gene cause hereditary sensory neuropathy type I, an autosomal dominantly inherited disease, and these mutations confer dominant-negative effects on SPT activity. Additionally, SPT is suggested to be a key enzyme for the regulation of sphingolipid levels in cells because regulation of sphingolipid synthesis at the SPT step prevents a harmful accumulation of metabolic sphingolipid-intermediates including sphingoid bases and ceramide. Excessive ceramide have been associated with type 2 diabetes mellitus (T2DM), dyslipidemia, and atherosclerosis[[1].