For instance, inhibiting the NLRP3 inflammasome activation in macrophages has been shown to prevent the transformation of fibroblasts into myofibroblasts [28], and specific deletion of Doublecortin-like kinase 1 (DCLK1) in macrophages has demonstrated a reduction in cardiac hypertrophy and myocardial fibrosis [29].TN-C, a profibrotic and proinflammatory modulator, not only weakens myocardial cell adhesion to connective tissues but also plays a crucial role in myofibroblast recruitment and aggregation [30–32]. This evidence concerns the gene DCLK1 and cardiac hypertrophy.