“…Beyond the role of GNB3 pathogenic variants in the etiology of CSNB1H, [8] Siffert and colleagues [78], described the c.825C>T (rs5443) polymorphism in exon 10 of the gene as linked to the expression of a shortened splice variant, Gβ 3 s, whose translated protein is characterized by the deletion of 41 amino acids, responsible of enhanced G-proteins signal transduction [78]. The c.825C>T polymorphism is associated with an increased risk of hypertension [78][79][80][81], obesity [59,82], diabetes [83], metabolic syndrome component [84,85], depression [86,87], seasonal variations in mood and behaviors [88], functional dyspepsia [89,90], stroke [91,92], arrhythmia [93], coronary artery disease [94,95], and other cardiovascular phenotypes [96][97][98][99]. In addition, duplication and overexpression of GNB3 gene is responsible for a syndromic form of childhood obesity [59,100].…”