Here, we found that Kindlin-2 interacts with histone methyltransferase supperssor of variegation3-9 homolog1 (SUV39H1) and recruits it to GATA4 promoter, leading to the enrichment of the di- and tri-methylation of H3K9, which in turn contributes to silencing of GATA4. Further, targeted deletion of Kindlin-2 in heart tissue of mice induced cardiac hypertrophy and that this pathological process can be accelerated by ISO-treatment. The gene discussed is SUV39H1; the disease is cardiac hypertrophy.