Studies of the splicing regulator of survival of motor neuron 2 (SMN2) gene, whose aberrant splicing contributes to disease severity in spinal muscular atrophy patients, by the deletion or mutation of the SMN1 gene 87, 88, found that overexpression of SRSF2 reduces SMN2 exon 7 inclusion by binding to a 10 nt RNA sequence surrounding the branch-point, located upstream of the 3′ splice site (3′ SS), thus promoting the selection of the 3′ SS 89-91. The gene discussed is SMN2; the disease is spinal muscular atrophy.