In recent years, numerous clinical studies have suggested a causal relationship between statin useand new-onset diabetes (NOD), which has greatly impacted the clinical use of statins.7,8 To solve this puzzle, we have speculated that low-density lipoprotein receptor (LDLR) may play a role in the pathological process of statin-associated T2D.9,10 Briefly, statins may enhance LDL-C intake by pancreatic islets via upregulation of LDLR; subsequently, exogenous cholesterol may impair the function of pancreatic islets, resulting in an increased risk of T2D. Here, LDLR is linked to dentatorubral-pallidoluysian atrophy.