IL-6, epithelial growth factor and vascular endothelial growth factor activate STAT3, thereby promoting increased expression of the anti-apoptotic Bcl-xL protein, which induces tumor cell survival, and preventing the synthesis of cytokines and growth factors that prevent the maturation of dendritic cells and decrease the recruitment capacity of CD8+ and NK cells. The gene discussed is BCL2L1; the disease is neoplasm.