Moreover, recent publications have shown that Akt and SETDB1 not only have the ability to directly interact [74], whereby SETDB1 promotes Akt signalling and directly represses pro-apoptotic gene transcription [75], but inducing this interaction also showed increased tumorigenesis in both NSCLC cell lines and mice models [76, 77]. This evidence concerns the gene AKT1 and non-small cell lung carcinoma.