Other mechanisms to promote constitutive PD-L1 expression in cancer cells included PTEN deletions, PI3K and/or AKT mutations, EGFR mutations, MYC overexpression, CDK5 disruption, and an increase in PD-L1 transcripts stabilized by truncation of the 30 UTR of this gene [65–69]. The gene discussed is CD274; the disease is cancer.