Furthermore, in the context of insulin resistance, whereby the canonical phosphatidylinositol 3-kinase (PI3K)/Akt metabolic pathway of insulin signalling is inhibited to various degrees, the Ras/Raf/Map kinase mitogenic pathway of insulin is undisturbed and possibly upregulated, leading to increased insulin-stimulated activation of FTase with subsequent increases in the amounts of farnesylated Ras [8,9]. The gene discussed is INS; the disease is Insulin resistance.