Another study of small-molecule inhibitors of histone methyl-transferases (HMTs) showed that chaetocin, a fungal toxin that inhibits four main mammalian HMTs (G9a, GLP, SUB39H1, and SETDB1), had a synergistic effect with 5-azadC in reactivating FMR1 in neural stem cells (NSCs) and neurons derived from FXS-iPSCs [66]. This evidence concerns the gene FMR1 and fragile X syndrome.