This fact correlates well with evidence that knockdown of p54nrb/NONO in the retina specifically induces splicing defects and altered expression of the rhodopsin gene [42], and the observation that spontaneous upregulation of PSPC1 and SFPQ could not rescue the behavioral deficits caused by NONO ablation in mice nor the intellectual disabilities caused by NONO mutations in humans [44]. The gene discussed is SFPQ; the disease is Intellectual disability.