This glycosylation of Bmal1 further promoted the binding of Clock to Bmal1, which upregulated Class E basic helix-loop-helix protein 41 (Bhlhe41) and DnaJ homolog subfamily B member 4 (Dnajb4) expression and led to ubiquitination and degradation of mitochondrial Na+/Ca2+/Li+ exchanger (NCLX), thereby inducing mitochondrial calcium overload and subsequently leading to neuronal damage and cognitive impairment in diabetes. The gene discussed is BMAL1; the disease is diabetes mellitus.