The inherent mechanisms, which have been shown to result in constitutive expression of PD-L1 by tumor cells, consist of alterations in the PTEN/PI3K/AKT pathway (65, 107), MYC overexpression (108), EGFR mutations (40), CDK5 truncation (109), and elevated PD-L1 transcripts stabilized by disruption of the 3-untranslated region (UTR) of this gene (110). The gene discussed is PTEN; the disease is neoplasm.