The physiology of aldosterone is relatively well understood. There is considerable epidemiological evidence that aldosterone has a role in the development of hypertension and other cardiovascular diseases. Even within the physiological range, increased plasma aldosterone levels predispose to development of hypertension [70]. Increased aldosterone levels in adulthood may be determined by conditions early in life such as foetal growth [71]. While plasma aldosterone and aldosterone to renin ratio were found to be heritable phenotypes, common polymorphisms in the CYP11B2 gene explained only partially variations in aldosterone levels [72] and [73]. This is akin to the previous experience with ACE and AGT levels and like before a large number of studies have been performed in recent years and these were meta-analysed by Sookoian et al. [74]. The evidence from the meta-analysis was borderline for association between hypertension (qualitative trait) and the C-344T variant of CYP11B2 and no association seen with systolic and diastolic blood pressure (quantitative trait). In any meta-analysis, the results depend on the constituent studies, and this is true of most of the studies included here and all the reasons mentioned above are applicable. Like other candidate genes, aldosterone synthase is an attractive target, and it is likely that evidence for association may come from studies of rare or structural variants in this locus.