MECP2 knockdown in mice rendered them incapable of tolerating increased H3K9 levels and deteriorated their Rett phenotype, whereas normal mice were able to deal with increased H3K9 methylation, suggesting a possible correlation between Rett syndrome and the H3K9 methylation mark, which is related to SETDB1 activity [149]. The gene discussed is SETDB1; the disease is atypical Rett syndrome.