The “pathway-selective hepatic insulin resistance” hypothesis states that during hepatic insulin resistance, Akt does not sufficiently activate Foxo1 to suppress gluconeogenesis; however, Akt maintains activation of the mTORC1 protein-kinase complex and the sterol regulatory element-binding protein 1c (SREBP-1c) transcription factor to enhance lipid synthesis. This evidence concerns the gene AKT1 and Insulin resistance.