The metabolic transition that accompanies feeding depends on insulin, which promotes the phosphorylation and activation of AKT protein kinases. AKT kinases modulate metabolism through several downstream pathways, one of which involves phosphorylation and inactivation of forkhead box O (FOXO) transcription factors. In the liver, FOXO1 induces the transcription of genes encoding gluconeogenic enzymes, and this activity is suppressed by the insulin–AKT pathway after feeding. In the current model of hepatic metabolism, AKT is an obligate insulin signalling intermediate. However, Lu et al. now show that mice livers can respond to nutrients and insulin signalling even in the absence of AKT when Foxo1 is also deleted. Rather than mimicking a state of continual insulin presence, liver-specific deletion of Foxo1, or Akt and Foxo1, did not suppress the expression of gluconeogenic genes from fasting to feeding, which suggests that another pathway, that is independent of AKT, can mediate the response to insulin.