These results highlighted the functional importance of FoxO3A S12 and S30 residues, together with the activation of pathways dictating their phosphorylation (Fig. 6c), in cancer cell resistance to metabolic stress, and prompted us to evaluate the inhibition of the MEK/ERK and/or the AMPK pathway in HCT116-FoxO3A+/+ cells cultured in LG conditions. This evidence concerns the gene MAP2K7 and cancer.