Of particular interest is the fact that induction of late-INa is involved in the development of heart failure and cardiac arrhythmias.21,29,30 Furthermore, drugs that act in part via late-INa inhibition are effective in animal models of heart failure.32,33 Our use of tetrodotoxin as a positive control for late-INa inhibition demonstrates that tetrodotoxin reduced NLRP3 inflammasome activation and improved functional recovery to the same extent as empagliflozin in an acute model of cardiac injury where late-INa is induced and the NLRP3 inflammasome is activated. The gene discussed is NLRP3; the disease is cardiac arrhythmia.