In SMA animal models, new treatments like the Ca(v)2.1/Ca(v)2.2 channel modifier, R-roscovitine, and a cyclin-dependent kinase 5 (Cdk-5) inhibitor that prolongs voltage-gated calcium channel openings, have been demonstrated to enhance NMJ construction and boost survival [104]. This evidence concerns the gene CDK5 and proximal spinal muscular atrophy.