 This follow-up strategy also allowed an active pharmacovigilance procedure, with side effects promptly reported to the GPs, which prevented the occurrence of difference in compliance among the various antihypertensive treatments. In addition, this kind of follow-up allowed by means of pharmacogenetic studies to demonstrate that the occurrence of side effects may be predicted from individual genotype 32. Indeed, we have recently reported that in patients bearing β2AR gene Glu27 variant or the β3AR gene Arg64 variant there was a larger occurrence of hypertriglyceridemia, alone or in combination with elevated cholesterol levels. Furthermore, the β2AR Glu27variant significantly associates with hypetriglyceridemia in a cumulative fashion. The risk of developing this side effect after β-blockade was four-fold higher in patients homozygous for the β2AR Glu27 variant than in β2AR27Gln allele. This result not only allowed the identification of patients at high risk to develop metabolic complications to chronic β-blockade treatment, but also contributed to elucidate the pathophysiological mechanisms which mediate these side effects, raising the possibility to prevent them. 