Using R270X and G273X mouse models, the breaking point was shown to be due to the disruption of an AT-hook 2 HMGA1 (high mobility group)-like domain in MeCP2 that was found to be critical for chromatin maintenance and α-thalassemia mental retardation X-linked protein (ATRX) localization in the nervous system (Baker et al., 2013), underscoring again the multifaceted role of MeCP2 in chromatin organization. This evidence concerns the gene MECP2 and thalassemia.