In sorbitol-stressed HeLa cells, the entry of SRPK1 into the nucleus induced the hyperphosphorylation of SR proteins, thus becoming inhibitory to the splicing of a reporter gene [9], while genotoxic treatments of human neuroblastoma cells resulted in the nuclear localization of SRPK2 and promoted changes in the splicing pattern of genes involved in DNA repair, cell cycle control, and apoptosis [13]. This evidence concerns the gene SRPK1 and neuroblastoma.