Apart from genetic amplifications and the increase of stabilized PD-L1 transcripts by truncation of CD274- 3’ UTR [4], PD-L1 over-expression in cancer cells has been related to the aberrant expression of different protein kinases, including constitutive activation of Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling, PTEN deletions, PI3K and/or AKT mutations, EGF receptor mutations, MYC overexpression and cyclin-dependent kinase 5 (CDK5) disruptions [4] (Figure 3). This evidence concerns the gene AKT1 and cancer.