Several factors can lead to the persistent expression of PD-L1 and/or PD-L2 on tumor cells by, for instance, upregulation by cytokines, chromosomal copy gain [21], disruptions of the PD-L1 3′-untranslated region [22], aberrant activity of pathways mediated by phosphoinositide 3-kinase (PI3K) and protein kinase B (PKB, AKT), epidermal growth factor receptor (EGFR), cyclin-dependent kinase 5 (CDK5), and Janus kinase 2 (JAK2) [21,23], MYC overexpression [24], and viral proteins, e.g., Epstein–Barr virus latent membrane protein 1 (EBV LMP1) [25]. This evidence concerns the gene AKT1 and neoplasm.