Furthermore, it was shown that although C5a did not modify cancer cell proliferation in- vitro, it induced endothelial cell chemotaxis, blood-vessel formation and favoured the generation of the immunosuppressive microenvironment required for tumour growth by promoting myeloid-derived suppressor cells and immunomodulators, namely arginine-1 (ARG1), cytotoxic T-lymphocyte associated protein 4 (CTLA-4), IL-6, IL-10, lymphocyte-activation gene 3 (LAG3) protein and programmed death-ligand 1 (PDL1) [144]. The gene discussed is C5; the disease is neoplasm.