For example, serological testing has been so far restricted by different sensitivity, specificity, and overall performance of assays that are applied in the diagnosis and are targeted on endomysium (EMA), tissue transglutaminase (TGA), and deamidated gliadin peptides antibodies (DGPA).4 Furthermore, up to 10% false-negative diagnoses of CeD are caused by seronegative CeD.5 Additionally, as most assays target antibodies of the IgA class, they do not help evaluate individuals who have an IgA deficiency (about 7% of patients with CeD). This evidence concerns the gene CD79A and cranioectodermal dysplasia.