Recent reports have revealed that CD4+ Th cell subsets have the ability to alter their gene expression pattern in response to extracellular stimuli. We previously highlighted the plasticity of Th1 cells by demonstrating that Th1 cells gain the capacity to produce IL-3, IL-9, IL-13 and granulocyte macrophage colony-stimulating factor in response to antigen, IL-2 and IL-18, and based on their unique function, we designated these activated Th1 cells as ‘super Th1 cells’. However, the precise molecular mechanism underlying IL-13 production by super Th1 cells has not been elucidated. Here, we show that the GATA-binding protein 3 (Gata3) is essentially required for Il13 gene expression in super Th1 cells. Gata3 is synergistically induced in T-box expressed in T-cells (T-bet)-expressing Th1 cells when co-stimulated with anti-CD3, IL-18 and IL-4 through the activation of nuclear factor of activated T cells, nuclear factor kappa-light-chain-enhancer of activated B cells and signal transducer and activator of transcription 6, respectively. However, Gata3 induction is not satisfactory, and additional TCR or anti-CD3 signaling is prerequisite for triggering IL-13 production by Gata3 plus T-bet-expressing Th1 cells. These findings suggest that Gata3, which is not originally expressed in Th1 cells, alters the cytokine production profile by Th1 cells.