Here we used primary murine macrophages, human monocyte cell lines, and primary monocytes from FMF patients in conjunction with bacterial toxins or effectors or chemical inhibitors, native PAGE, immunoblotting with phospho-specific pyrin antibodies, and siRNA knockdowns to determine if PPP activity is required to dephosphorylate oligomeric pyrin and positively regulate inflammasome assembly in response to the inactivation of the Rho-PKN axis. This evidence concerns the gene PKN1 and familial Mediterranean fever.