On one hand, exogenous stimulus delivered by the pro-inflammatory cytokines in the inflammatory microenvironment can trigger the receptor mediated signaling molecules within the tumor cells (including NF-κB, MAPK, PI3K, mTOR, and JAK/STAT) that promote cell proliferation, and induce PD-L1 expression as well [22]. The gene discussed is SOAT1; the disease is neoplasm.