They suggested that because mice deficient in this enzyme were unable to produce nitric oxide, to form organized granulomas or to control Paracoccidioides multiplication and therefore died a short time after infection having produced high levels of Th1 (IL-12, IFN-γ and TNF-α) and Th2 (IL-4 and IL-10) cytokines. The gene discussed is IL4; the disease is infection.