CAMK2D and myotonic dystrophy type 1: One possible reason for this modest splicing alteration in the cerebellum of human DM1 is that fetal splicing isoforms of some genes are already dominantly expressed in human adult cerebellum and thus there is no room for any detectable difference of fetal isoforms between DM1 and control samples (e.g. CAMK2D in which fetal δ9 isoform is almost exclusively expressed in both disease control and DM1 cerebellums relative to fetal brain (Figure 3E)).