These complex trends were observable in the present dataset, as well, and manifested themselves by the induction of M2a (via IL-4/IL-13) and M2c (via IL-10) polarized populations of cells with tumor-promoting activities that encompassed type II inflammatory/Th2 responses in M2a cells, and, matrix deposition, ECM remodeling and suppression of immune responses in M2c cells (28). The gene discussed is IL4; the disease is neoplasm.