While IDC16-mediated splicing modulation has been tested only for few genes, a likely explanation for this difference of splicing inhibition behavior could be that the viral RNA has to escape the splicing machinery during later stages of infection to produce viral particles containing full-length unspliced pre-mRNA, whereas most cellular genes have constitutive exons that contain redundant binding sites for SR proteins. The gene discussed is RNPS1; the disease is infection.