Evidence is beginning to accumulate that not only development and progression of left ventricular hypertrophy (LVH) in hypertension is genetically predisposed, but its regression during therapy has several genetic determinants. Renin-angiotensin system (RAS) is generally considered to be the major contributor to LVH development. I/D polymorphism of angiotensin-converting enzyme (ACE) gene was shown to determine plasma ACE concentrations and LVH severity in hypertension. Several studies have also documented association of angiotensin II type I receptor gene (AT1R) polymorphism (A1166C) with LVH. Impact of angiotensinogen (ATG) genetic polymorphisms (-6G/A or M235T) in LVH is not so well established. Gene-gene interactions between these genes are also described. Since pharmacogenetic approach has been introduced to testing of antihypertensive drug efficacy, the influence of RAS genetic polymorphisms on LVH regression during treatment was also analyzed in several studies. The data obtained nowadays are rather controversial. Large proportion of studies documented lower LVH regression in patients carrying D allele (or DD genotype) of ACE gene. C allele of AT1R gene is also shown to influence LVH reversal during treatment. However, major clinical studies concerning effects of different drugs on hypertensive LVH did not include genetic investigations; the existing data are obtained on rather small patient samples, do not take into account gene-environmental interactions, and need to be tested in larger trials.