Indeed, enhanced cAMP-dependent protein kinase activity and Wnt signaling in stromal cells/osteoblasts may contribute to the tumor-like phenotype of bony outgrowths in NOMID patients15, 16; and hyper-activation of the NLRP3 inflammasome is presumed to promote chondrocyte apoptosis, thereby contributing to deafness in CAPS patients6, 17. The gene discussed is NLRP3; the disease is CINCA syndrome.