A tumor-friendly TME would probably present one or more of the following features: PI3K/AKT and MEK1/2 signaling via C3a-C3aR and/or C5a-C5aR axes, JAK2/STAT3 activation driven by tumor-deposited C3 fragments, promoting growth/metastasis, anti-apoptotic effects via CD59-mediated inhibition of terminal complement complexes, C5a-induced Akt-dependent oncogenic RGC-32 expression, overexpression of CD55, CD46, and CD59 on tumor cells, Factor H overexpression, enhancing stemness (via LSF-1) and angiogenesis. This evidence concerns the gene STAT3 and neoplasm.