proposed that hyperaccumulation of InsP6 in neuronalcells of PCH patients might be a mechanistic cause of this diseaseby chelating iron ions.21 In fact, allInsP species which possess the 1,2,3-phosphorylated motif might becapable of binding iron ions.62 In contrastto their reported 3–4-fold increase of [3H]InsP6 levels (normalized against total tritiated PIPs) in MINPP1–/– HEK293cells compared to WT cells, we only observed a slight increase usingthe same cell line but normalizing against packed cell volume. This evidence concerns the gene MINPP1 and pontocerebellar hypoplasia.