Interestingly, pharmacological inhibition of Caspase 1 and NF-κB led to a complete abrogation of CD1c+ cDC activation and IL-1β expression in response to dsDNA-IgG complexes, while drugs specific for the NLRP3 inflammasome, previously involved in Mo activation in RA (32), led to a partial and less significant effect, suggesting that additional nonredundant inflammasome sensors and NF-κB might be involved in the process. This evidence concerns the gene NFKB1 and rheumatoid arthritis.