Mutant IDH enzymes may promote tumor growth through mechanisms other than the reported inhibition of TET enzymes: Thus, mice expressing endogenous mutant IDH1 display reduced numbers of hematopoietic stem cells, in contrast to TET2-deficient mice; mutant IDH1 downregulates the DNA damage sensor ATM by altering histone methylation, determining impaired DNA repair, increased sensitivity to DNA damage, and reduced hematopoietic stem cell self-renewal, independent of TET2; ATM expression is decreased in primary IDH1-mutants AMLs [91]. Here, TET2 is linked to neoplasm.