SETD2 and central nervous system cancer: There is, however, a growing awareness of the importance of disruption of K36 methylation, and the enzymes involved in its deposition, such as SETD2, NSD1, and NSD2 in pHGG, where 15% of histone wild type cortical high grade gliomas bear deleterious mutations in SETD2 [134], and H3K36 methylation is affected by H3.3 G34R/V mutation in an additional ~18% of cortical gliomas.