For instance, mutations in TP53 and ATRX are the underlying denominator in defining which IDHWT and IDHMUT gliomas respond to radiotherapy [70]; the overexpression of BCAT1 in IDHWT AML leads to an IDHMUT-like DNA hypermethylation phenotype [71], and additional mutations in DNMT3A cause reduced levels of DNA hypermethylation in IDHMUT AML samples [74]. Here, DNMT3A is linked to acute myeloid leukemia.