CD4 and colitis: With the administration of EGCG and IFN-γ in CD4+ T cells (i.e., primary CD4+ T cells from C57Bl/6 mice and a human leukemic CD4+ T cell line of Hut 78 cells) and non-CD4+ T cells (i.e., HepG2 cells), the study indicated that EGCG alternatively enhanced the signal transducer and activator of transcription (STAT) 1 phosphorylation, but inhibited the STAT1 homodimer formation via the Src pathway, but not the Janus kinase (JAK) 1/2 pathway, ultimately promoting the apoptosis of IFN-γ-induced CD4+ T cells and benefiting the T cell-related colitis [93].