Glycosylation of proBNP at threonine 71 prevents cleavage to form bioactive BNP1-32 and NT-proBNP; in obese patients with chronic heart failure, it was demonstrated that proBNP, not glycosylated at threonine 71, was decreased; owning to this lack, authors concluded that O-glycosylation is relevant to reduce plasma concentrations of BNP/NT-proBNP in obesity (Lewis et al., 2020). This evidence concerns the gene NPPB and obesity due to melanocortin 4 receptor deficiency.