The 22q11 chromosomal deletion syndrome (22q11 DS) is associated with learning disabilities and a complex neuropsychological profile. Previous findings have suggested that executive attention deficits might underlie other neurocognitive anomalies. We administered the child Attention Network Test (ANT) to 52 children ages 5.0 to 11.5, 32 22q11 DS children (19 girls) and 20 controls (13 girls) and assessed the efficiency of segregated executive, orienting, and alerting networks. We hypothesized that 22q11 DS children have impaired executive network efficiency as compared to control siblings. The internal validity of the child ANT was confirmed for this population. Analysis of variance results showed significant main effects for flanker and cue types and no interaction effect in either 22q11 DS children or control siblings. Compared to control siblings, 22q11 DS children had significantly larger (less efficient) executive network scores, significantly increased errors on only incongruent trials, and a significant correlation between executive network scores and accuracy. The implications of these findings for future neurocognitive studies of 22q11 DS children are considered.The 22q11 deletion syndrome (22q11 DS) results from a meiotic deletion of DNA at the q11.2 site on chromosome 22 and its estimated prevalence is 1:4,000 (du Montcel, Mendizabal, Ayme, Sevy, & Philip, 1996). In over 90% of cases the deletion is not transmitted (Morrow et al., 1995). Congenital anomalies of widely varying severity can be associated with this condition and might include heart defects, immunologic deficits, craniofacial dysmorphologies, and velopharyngeal defects such as overt or submucous cleft palate (e.g., Ryan et al., 1997). Prior to identification of a single associated deletion, different clinical labels were used to indicate a given child's congenital anomalies, including DiGeorge Syndrome (primary immunologic deficit), Velo-Cardio-Facial-Syndrome (VCFS; velopharyngeal, heart, and facial anomalies), and Conotruncal Anomaly Face Syndrome (primary heart defect with facial dysmorphologies). Whereas the physical phenotype is heterogeneous, the neurocognitive profile is far more consistent. Researchers have estimated that 90% to 100% of 22q11 DS children are learning disabled (e.g., Lipson et al., 1991;Shprintzen, Goldberg, Young, & Walford, 1981) and hypotonic, with gross and fine motor dyscoordination, associated expressive language delays, attention impairment, and behavioral anomalies . Frank mental retardation is relatively rare and may be associated with prolonged anoxia during early cardiac failure. Of urgent concern, approximately 25% of 22q11 DS children are estimated to develop early adulthood schizophrenia (Murphy & Owen, 1996; Pulver et al., Copyright © 2004 The neurocognitive performance of 22q11 DS children is notably complex however and visuospatial memory deficits alone are unlikely to fully explain their profiles. In fact when a broader complement of abilities was examined additional areas of deficit were revea...