It appears that several pathways can lead to pathologic inflammatory responses in cutaneous leishmaniasis, including extensive cell lysis leading to inflammasome activation and IL-1β production [6,27–29], infection with more virulent strains of the parasite [5] and the lack of regulatory cytokines such as IL-10 leading to an IL-1β and IL-17 mediated pathology [7,30]. The gene discussed is IL1B; the disease is cutaneous leishmaniasis.