This antedated the finding in 1999, when NICHD-supported scientists discovered that most classic Rett syndrome cases are caused by a mutation within the methylcytosine-binding protein 2 (MECP2) gene on the X chromosome, with the view emerging that disruption of the RTT gene alters the normal developmental expression of various other genes, some of which must account for the neurologic phenotypes associated with this disorder [39]. The gene discussed is MECP2; the disease is atypical Rett syndrome.