Notably, the pharmacological inhibition of NLRP3 with MCC950, the blockade of IL-1 signaling with the IL-1 receptor antagonist anakinra, and the genetic silencing of Nlrp3, Casp1, or Il1r1 all attenuated these electrophysiological abnormalities, reinforcing the centrality of the NLRP3–IL-1β axis in arrhythmia pathogenesis [154]. This evidence concerns the gene NLRP3 and cardiac arrhythmia.