BTNL8 and cranioectodermal dysplasia: Participants who are homozygous for the deletion can only express the truncated BTNL8*3 fusion protein, which lacks the BTNL3-IgV extracellular domain required for maintaining the duodenal TCR of Vγ4+ γδ T cells, which we hypothesised could increase CeD risk [21,29,31,41].