Briefly, tumor cells can activate PD-L1 expression via the following mechanisms: (1) alterations of genes, including EGFR, ALK fusions, KRAS, MYC, PTEN, and p53; (2) exogenous inflammatory cytokines, such as interferon-γ; (3) PD-L1 amplification; and (4) disruption of the 3′-untranslated region of the PD-L1 gene [75]. Here, KRAS is linked to neoplasm.