Alternatively, it may be that the accumulation of rare variants confers the most risk for ADHD rather than variation in common SNPs studied here. The initial evidence suggesting SLC9A9 as a potential candidate for ADHD came from a pericentric inversion of chromosome 3 identified in a single family, for example. 18 Elia et al 27 found no over representation of copy number deletions or insertions in ADHD youth but found that inherited copy number variations were located in genes with prior evidence of involvement with neuropsychiatric conditions related to ADHD.
