This inflammatory death program, mediated by the NLRP3/caspase-1/GSDMD axis, promotes release of IL-1β and IL-18, sustaining inflammation and cardiomyocyte loss associated with adverse ventricular remodeling and progression toward CHF (Chen et al., 2022; Zeng et al., 2020; Zhang L. et al., 2024). This evidence concerns the gene IL1B and congestive heart failure.