Previous studies showed that Bcl-2 and Bcl-xL were decreased whereas Bax, cytochrome C, and caspase-3 were not increased in young about 4 weeks old but increased in mature hypertensive brain indicating that hypertension activated the mitochondrial-mediated Caspase-dependent apoptotic pathway and suppressed the Bcl-2 pro-survival pathway in the brain (Li et al., 2012, 2016). This evidence concerns the gene BCL2L1 and hypertensive disorder.