Our present study demonstrated that the upregulation of mucin-type O-glycosylation correlated with the progression of cardiac hypertrophy and HF; this may contribute to the increase in sialylated O-glycan at Thr71 close to the processing site, resulting in the inhibition of proBNP conversion to bioactive BNP-32 by hindering the binding of a processing protease, furin [48]. The gene discussed is NPPB; the disease is cardiac hypertrophy.