Myocardial oxidative stress facilitates apoptosis and inflammation, leading to cardiac fibrosis and promoting cardiac dysfunction.41 Myocardial inflammation is influenced by redox-sensitive transcriptional factors such as NFkB.42 Our transcriptome analysis demonstrated that canagliflozin suppresses several redox-sensitive pro-inflammatory and pro-apoptotic pathways in hCM, such as those of TNF-α and IL-1 as well as, crucially, on NFkB activity. Here, NFKB1 is linked to fibrosis.