MYT1L and obesity due to melanocortin 4 receptor deficiency: We identified deletions of 2p25.3, Xp and 22q11.21 that overlap with deletions identified in previous studies of CNV in CP (Table 1).9–11 Deletions of 2p25.3 [OMIM: 616521] encompass a syndrome of ID, obesity, ASD, attention deficit hyperactivity disorder (ADHD) and delayed psychomotor development.19 The neurological phenotypes associated with 2p25.3 deletions have been linked with haploinsufficiency of MYT1L and that gene was also deleted in the individual in this study, however it was not expressed in LCL19 (Table S4).