However, phosphorylation of AKT and S6 was not changed in the lung adenocarcinoma A549 cells with the knockout of the SESN1 and/or SESN2 genes (Figure 4C–4D), indicating that pro-oncogenic signaling pathways activated during carcinogenesis may overcome the need for SESTRINs to support the high activity of AKT. The gene discussed is AKT1; the disease is lung adenocarcinoma.