In this case, the modification of Cys664 abolished the Krüppel-like factor 5 (KLF5) promoter binding to SP-1 and inhibited cardiac hypertrophy (because when SP-1 is coupled with KLF5 promoter, it has a pro-hypertrophic effect in the heart) (Figure 4). The gene discussed is KLF5; the disease is cardiac hypertrophy.