The effect of vitamin C treatment in FH and SDH mutant malignancies has not yet been reported, however the responsiveness of IDH mutant leukemia cells to vitamin C (despite being depleted of α-KG) suggest that enhancing any residual amount of functional wild-type TET or JHDM activity, even in the presence of inhibitory oncometabolites, could be sufficient to restore epigenetic differentiation cues and erase aberrant DNA and histone hypermethylation phenotypes. Here, IDH1 is linked to leukemia.