Currently, GPP is essentially considered to be a distinct entity from plaque psoriasis, with a distinct genetic and pathogenic profile.5, 11 Hussain et al. found that in patients with a mutation in the interleukin-36 receptor antagonist (IL-36RN) gene, the onset of GPP tends to occur earlier, associated with a higher risk of systemic inflammation and a lower association with plaque psoriasis.12 The gene discussed is IL36RN; the disease is psoriasis 14, pustular.