Patients with DH frequently exhibit elevated levels of interleukin‐8 (IL‐8), a cytokine that promotes the influx of neutrophils into the dermis and the formation of secondary vesiculo‐bullous lesions, as well as an increased expression of IL‐17 and IL‐36 correlated with the activity of the disease [6, 7]. Here, IL17A is linked to dermatitis herpetiformis, familial.