This is probably related to the activation of feedback compensatory loops leading to tumor cell resistance like the up-regulation of IRS-1 protein levels and the induction of IRS-1 phosphorylation [19], the activation of both Akt phosphorylation via mTORC2 [30–32] and MAPK pathway via S6K/PI3K/Ras pathway [20]. The gene discussed is AKT1; the disease is neoplasm.