Notably, HIES also exists in an AR form that may be caused by defects in either TYK2, dedicator of cytokinesis (DOCK)8, or phosphoglucomutase (PGN)3, although these present with a somewhat different phenotype, including a more pronounced tendency toward cutaneous viral infections and without the somatic phenotype characteristic of AD HIES resulting from STAT3 mutations (78, 93–95). This evidence concerns the gene TYK2 and viral infectious disease.