As PROM1 is highly expressed in the lungs (Figure 4B) and associated with the production of IL-22 as well as IL-1β induces IL-22 [87], to evaluate the PROM1 and CLEC7A variants described in this study in PCM patients, future work should contribute to understanding mechanisms involved in resistance or susceptibility to the disease, revealing novel targets for treatment of PCM. This evidence concerns the gene IL1B and paracoccidioidomycosis.