In this way, the recruitment of Bcl6 to the Ifnγ locus prevents an excessive amount of IFN-γ in Th1 culture.8 Potentially, this action may limit the immune pathology and autoimmunity caused by excessive Th1 signals; however, further studies are required to determine if this molecular mechanism is relevant in vivo and disrupted during immune pathology. Here, IFNG is linked to Autoimmunity.