Similar to IRBIT, CA8 is also a non-enzymatic competitor of IP3 that binds to IP3R and interestingly, recessive mutations in CA8 cause a congenital ataxia with intellectual disability, possibly acting by disinhibiting the interaction between IP3 and the IP3R, allowing extra Ca2+ to be released from IP3-sensitive stores (Turkmen et al., 2009; Kaya et al., 2011). The gene discussed is ITPR1; the disease is Intellectual disability.