Western blotting showed the nuclear level of NFκB-p65 was increased by 76% in the myocardium of infected/untreated (Fig 7Aa & 7Ab, *p<0.05) mice, and normalized to control levels in infected/SRT1720-treated mice (#p<0.05), thus suggesting that SIRT1 might regulate NFκB activation in CCM. The gene discussed is SIRT1; the disease is cerebral cavernous malformation.