One of the mechanisms firstly shown to cause insulin resistance was the accumulation of secondary products of lipid metabolism, such as diacylglycerol, ceramides, and long-chain acetyl coenzyme A. The accumulation of such products in myocytes was shown to activate serine/threonine kinases like c-jun N-terminal kinase (JNK), IκB kinase (IKK), and protein kinase C (PKC), conducting to serine phosphorylation and consequent inactivation of the insulin receptor and its substrates [4–7]. The gene discussed is INSR; the disease is Insulin resistance.