Recently, an epigenetic therapy strategy based on HDAC inhibitors to modulate chromatin marks was used to improve in an animal model with Spinal Muscular Atrophy (SMA) the inclusion of the type II SMN2 exon 7, increasing the therapeutic efficacy of an antisense oligonucleotide (ASO)-splicing therapy [15]. The gene discussed is SMN2; the disease is proximal spinal muscular atrophy.