In this study, by identifying Id2 to be critical for reprogramming Treg cells towards a TH17 like phenotype in the context of inflammation, we have not only defined a hitherto unidentified mechanistic switch critical for inducing Treg plasticity, we have also identified a novel molecular target that can be potentially modulated in order to reinforce or undermine Treg stability in the context of autoimmunity and cancer. Here, ID2 is linked to cancer.