Mice with a targeted deletion of Fpr1 are significantly less vulnerable to the pathologic features of the secondary damage associated with BOS and induced by the activation of the NLRP3 inflammasome compared with the control, while IL-1β/IL-18 and Casp-1 KO animals were less susceptible than the WT but more than the Fpr-1 KO. This evidence concerns the gene FPR1 and Buschke-Ollendorff syndrome.