This is exampled by the induction of STAT1 and STAT3 by IFN-γ, whereby T cell differentiation is skewed toward Th1 by STAT1 and Th17 by STAT3, and that tumor cell proliferation might be restricted by STAT1 yet enhanced by STAT3—differential effects largely mediated by SOCS protein associations [89]. The gene discussed is STAT3; the disease is neoplasm.