The over-expression of PD-L1, promoted by oncogenic and constitutively activated signals, including epidermal growth factor receptor (EGFR), protein kinase B (AKT) and Kirsten rat sarcoma viral oncogene homolog (KRAS) pathways, is responsible for an innate (tumor cell intrinsic) resistance (109–113). This evidence concerns the gene AKT1 and neoplasm.