The detection of IL-36α and IL-36γ overexpression in lesional skin and peripheral blood samples from patients with GPP further supports the central role of IL-36 dysregulation in this condition (14, 73), and there is a strong association between loss-of-function mutations in IL36RN (producing faulty IL-36Ra protein) and increased susceptibility to GPP (36, 37, 46). Here, IL36A is linked to psoriasis 14, pustular.