Since an impairment in systemic glucose tolerance serves as a high risk for developing type 2 diabetes mellitus in humans, it is anticipated that the elucidation of the pathobiological relationship between the decrease in serine synthesis via the phosphorylation pathway, the diminishment of the insulin/IGF signaling pathway, and the impaired glucose tolerance in the human liver will provide new mechanisms related to impaired glucose tolerance and useful opportunities for its diagnosis and prevention. This evidence concerns the gene IGF1 and type 2 diabetes mellitus.