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]. The gene discussed is ZFP36; the disease is Intellectual disability.