Recent studies have indicated that the primary mechanisms by which TLR4/NF-kB exacerbates myocardial infarction encompass inflammation [123], oxidative stress [124], and pyroptosis—an inflammatory form of cell death that governs cardiomyocyte loss post-myocardial infarction—as well as apoptosis [125,126]. The gene discussed is NFKB1; the disease is myocardial infarction.