More importantly, it has been proven that activation of the NLRP3 inflammasome mediating the release of proinflammatory cytokines into CMs can promote the deposition of collagen and the formation of left ventricular (LV) hypertrophy, fibrosis, and diastolic dysfunction with normal ejection fraction, which further develops into heart failure with preserved ejection fraction (HFpEF), whereas others eventually develop into heart failure with reduced ejection fraction (HFrEF) [15, 16]. The gene discussed is NLRP3; the disease is heart failure.