Previous studies have demonstrated that increased levels of cytokines like IFN-γ (43) in the tumor microenvironment, along with the activation of the JAK-STAT (44), PI3K-Akt (45), and Toll-like receptor signaling pathways (46) can upregulate PD-L1 expression in both tumor and some immune cells, which enables tumor cells to evade immune surveillance (47). The gene discussed is SOAT1; the disease is neoplasm.