It is possible that some MINPP1-generatedInsPs (or the lack thereof) could be important contributing factorsin MINPP1-regulated processes, i.e., ER stress, endochondral ossification,and neuronal function.17,19,21 For example, it would be interesting to investigate if the hyperaccumulationof InsP5[3OH] or the absence of Ins(2,3)P2 andIns(2)P is partially responsible for causing PCH in patients withMINPP1 loss-of-function mutations.20,21 Ucuncu etal. This evidence concerns the gene MINPP1 and pontocerebellar hypoplasia.