The CNVs Exo2 designated as likely pathogenic comprise of 22% of our data. They were called likely pathogenic because they harbor genes having well-established association with abnormal phenotypes. Moreover, their genic content has been implicated in the process of neurological development, as mediators of neuroendocrine stress responses, to be expressed exclusively in the brain. However, none of the genes observed in the likely pathogenic CNVs was yet directly related to ID. We also observed a maternally inherited region which was involved with Chromosome 22q11.2 Duplication Syndrome. This region is also found deleted in the DiGeorge Syndrome and Emanuel Syndrome. Both IMS2186 syndromes are characterized by multiple congenital anomalies, significant developmental delay, and mental retardation. At the case 15, despite the location of ATP2B3 and FAM58A genes in Xq28, this region has not yet been implicated in ID per se. ATP2B3 gene encodes a calcium-transporting ATPase predominantly expressed in the brain, and mutations in the gene have been associated with increased plasmatic concentrations of aldosterone and reduced plasmatic potassium. Moreover, base substitution in ATP2B3 identified by exome sequencing in a family with X-linked congenital ataxia indicated the importance of calcium homeostasis in neurons. Nevertheless, the affected persons present neither mental retardation nor pyramidal tract involvement at their neurological examinations. On the other hand, mutations in FAM58A cause an X-linked dominant disorder known as STAR Syndrome. This syndrome presents facial dimorphism, toe syndactyly, telecanthus, anogenital and renal malformations. Nevertheless, patients with STAR Syndrome do not show ID. The proportion of CNVs classified as of unknown clinical significance was high in our study. According to researches, the ability to detect CNVs has far outpaced our ability to understand their role in a disease. Inheritance studies are the primary strategy recommended to estimate the role of such CNVs in pathogenicity. Nevertheless, it is often imprudent to attribute clinical significance to a CNV based solely on its inheritance pattern as a growing number of CNVs show an incomplete penetrance and also because de novo CNVs may represent benign variants. The clinical and genetic interpretation of the data acquired by CMA technologies still remains a challenge and often require further specific investigations.