Studies in murine models also showed that the small molecule HDAC inhibitor trichostatin A [47] prevented T1D symptoms through increased acetylation of histone H3, which was associated with increased expression of the CD4+ T cell-derived lymphokine interferon gamma (INF-γ) and its transcription factor Tbet/Tbx21 [48], highlighting the potential role of chromatin remodeling agents in the protection against the development of T1D. Here, IFNG is linked to type 1 diabetes mellitus.