Lastly, additional studies are underway to identify mechanisms that increase the frequency of Tregs, with some insights regarding tumor necrosis factor receptor-2 (TNFR2) and the TNFα pathway playing an important role in increasing the frequency of Tregs in AML patient samples[65], in addition to increased expression of IFNγ via IDO1 overexpression in mesenchymal stem cells[36]. This evidence concerns the gene TNFRSF1B and acute myeloid leukemia.