Our data strongly suggest that this neo-ARE induces ZFP36-mediated effect on the post-transcriptional control of SCL4A4. The consistent lack of any syndromic feature in all patients with this mutation is in striking contrast to the known syndromic phenotype associated with coding mutations in SLC4A4, i.e. severe renal and ocular involvement with intellectual disability [36]. This evidence concerns the gene SLC4A4 and Intellectual disability.