To exclude that these changes are merely a consequence of the degenerative process occurring in the spinal cord of hFUS+/+ mice rather than a cause of the degeneration itself, we analysed the alternative splicing of these specific pre-mRNAs in two other mouse models of motor neuron degeneration: the well-established G93A mouse model of ALS, and a Spinal and Bulbar Muscular Atrophy (SBMA) mouse model, where part of the human exon 1 Androgen Receptor gene carrying 113 CAG repeats had been inserted into the homolog region of the endogenous mouse gene23. This evidence concerns the gene AR and amyotrophic lateral sclerosis.