Interestingly, a recent unbiased RNA-sequencing-based assessment of global gene changes in SMN-depleted mouse tissues confirmed the specific missplicing of U12 snRNP-dependent genes, several of which are Ca2+ channel genes and may be upstream regulators of Cdk5 activity (Doktor et al., 2017), thus further highlighting Cdk5 as a potential pathological effector in SMA. The gene discussed is SMN1; the disease is proximal spinal muscular atrophy.