On the other hand, it has been reported that MEK inhibition leads to PI3K/Akt activation; Turke et al. demonstrated that this interplay is through a negative feedback on ErbB receptors; in the presence of a MEK inhibitor, ERK is inhibited and the T669 of EGFR a MAPK target site is blocked, increasing EGFR and ErbB3 tyrosine phosphorylation and upregulating the PI3K/Akt activation in lung cancer cells [18]. The gene discussed is AKT1; the disease is lung cancer.