The exact correlation between HS and Cx26 mutations and the interplay of gap junctions and inflammation remain to be elucidated; it is believed that HS might result from the hyperproliferative tendency of KID syndrome patients' epidermis, leading to follicular plugging, cyst formation, and rupture and spillage of keratin and glandular secretions into the subcutaneous tissue, causing an inflammatory response (55). This evidence concerns the gene GJB2 and KID syndrome.