Emerging evidence highlights the significant role of inflammation in myocardial remodeling, with cardiomyocytes and cardiac fibroblasts producing inflammatory cytokines such as TNF-α, IL-6, and IL-1β, which exacerbate myocardial hypertrophy, fibrosis, and ventricular stiffness, ultimately influencing the clinical course of HCM (11–13). The gene discussed is IL6; the disease is cardiac hypertrophy.