Specifically, recent preclinical studies showed that GSKJ4, a small molecule inhibitor of the histone H3K27 demethylases JMJD3 (KDM6B) and UTX (KDM6A), decreased tumor cell viability and increased H3K27me3 levels in glioma cell lines harboring the mutation of lysine to methionine substitution at codon 27 (K27M), and significantly extended survival of mice with K27M mutant glioma xenografts [160]. This evidence concerns the gene KDM6A and neoplasm.