Blocking survivin potentiated the inflammatory status of cancer cells (as indicated by an increase in IL-1β and TNFα expression), but significantly reduced the expression of immune suppression, angiogenesis, invasiveness and tumor growth-related markers, indicating that tumor microenvironment survivin (secreted by both obese ASCs and macrophages) promotes a pro-tumorigenic gene expression profile in HepG2 cells. Here, IL1B is linked to neoplasm.