From those, 182 patients had visible ITSA-1 chromosome aberrations from which accurate and definite diagnoses were possible. Of the remaining 123 cases, we contacted every family in order to explain about CMA as a new available genetic test potentially useful to explain the ID of the proband and also to offer the test to the family. The correct diagnosis of a neurological disorder is crucial for predicting the probands�� clinical follow up, to establish accurate prognostic, and to provide adequate genetic counseling. CMA technology is a relatively new strategy useful as an additional tool for genetic diagnosis. The method has been recommended as the first-tier diagnostic test for patients with global developmental delay, intellectual disability, autism spectrum disorders, and multiple congenital anomalies. In the current study, high-resolution CMA was carried out on 15 patients with ID, and relevant CNVs were found in 9 patients. From those, it was possible to propose the etiology of intellectual disability for 3 patients, which is consistent with other studies that have used this or similar technologies, and 16-Epiestriol reported improving the diagnostic yield up to 10�C25%. No changes in copy number were observed in six patients. Thus, it was not possible to suggest a genetic cause for the ID and high-resolution CMA was not useful to diagnose these cases. The possibility of testing these individuals with more sensitive or specific genomic technologies, such as next-generation exome sequencing could be a fruitful diagnostic approach in order to identify gene mutations that may be causing the observed phenotype. Moreover, ID is a polygenic complex and heterogeneous multifactorial trait, which remains a diagnostic challenge for human geneticists and heavily affected by environmental factors. We identified 4 pathogenic CNVs, including chromosomal imbalances associated with 17p11.2, Xq27.3, 18q11.1 and Xp22.33. Case 2 was a boy who presented a de novo microduplication at 17p11.2. Interestingly, the log ratio probe intensity on this region was compatible with a mosaic duplication affecting about 50% of cells. The region has been implicated in the Potocki-Lupski Syndrome. Additionally, microdeletion of this region has been associated with Smith- Magenis Syndrome. Gain or loss of genomic material on chromosome band 17p11.2 inevitably leads to phenotypes that include ID as a relevant trait.