In a previous study considering these factors in innate resistance to T. gondii, the authors insisted that SOCS3, a target of STAT3 that limits signaling via the pleiotropic cytokine IL-6, is upregulated in response to infection but is dispensable for the immune-inhibitory effects of T. gondii, suggesting a critical role for SOCS3 in suppressing IL-6 signals and promoting immune responses to control infection [22]. The gene discussed is STAT3; the disease is infection.