In addition, keratinocytes exposed to ultraviolet B irradiation, contact allergens or in the setting of psoriasis activate similar inflammasome pathways resulting in IL-1β production and subsequent neutrophil localization and activation (59–61), although there is support from mouse models that bone marrow-derived cells with isolated NLRP3 mutations are sufficient to induce IL-1β associated cutaneous autoinflammation (62). This evidence concerns the gene IL1B and psoriasis.