Involved in neurite outgrowth by regulating cell-cell adhesion via the N-cadherin signaling pathway. May act by regulating expression of protein-coding genes, such as N-cadherins and integrin beta-1 (ITGB1). Highly expressed in fetal and adult brain, predominantly in the cerebral cortex and the cerebellum. Also expressed in other tissues but to a lesser extent. The disease is caused by variants affecting the gene represented in this entry. A chromosomal aberration involving NEXMIF is found in patients with severe intellectual disability. Pericentric inversion inv(X)(p22.3;q13.2) with P2RY8 leading to inactivation of NEXMIF (PubMed:15466006). XLID98 transmission pattern is consistent with X-linked recessive inheritance (PubMed:23615299). In some cases, de novo heterozygous loss-of-function mutations have been found in affected females, while some female carriers are asymptomatic (PubMed:26576034, PubMed:27358180, PubMed:27568816). The female phenotype partially overlaps with the reported male phenotype but includes epilepsy as a relevant feature. The variability of disease manifestation in female carriers is probably due to skewed X inactivation with differential expression in the brain (PubMed:26576034, PubMed:27358180, PubMed:27568816).