IP3R-knockout studies have revealed that IP3R1-deficient mice die in utero or by the weaning period, and the survivors have severe behavioral abnormalities in the form of ataxia and epileptic seizures35, whereas IP3R2 and IP3R3 double knock-out mice exhibit hypoglycemia and deficits of olfactory mucus secretion, suggesting that these two isoforms play key roles in the exocrine physiology and perception of odors36, 37. This evidence concerns the gene ITPR2 and cerebellar ataxia.