Since the prevalence of endothelial dysfunction, metabolic disturbances, and hypertension remains increased in patients with controlled acromegaly compared to the general population, it has been suggested that specific traits of systemic inflammation are induced during GH/IGF-1 excess in active acromegaly and partially persist in controlled acromegaly, which may contribute to the development and persistence of CV comorbidities and hence increase the risk of macrovascular events in these patients (Figure 1) [21–24]. This evidence concerns the gene GH1 and acromegaly.