Tang’s study [13] showed that SRSF3 could regulate cellular senescence through TP53 alternative splicing; Ajiro’s study [7] found that SRSF3 could regulate the expression of 60 genes and 20 miRNAs in human osteosarcoma cells by the global profiling of the SRSF3-regulated splicing events; Kuranaga’s study [10] indicated that SRSF3 as a PKM splicer played a positive role in cancer-specific energy metabolism; Gautrey’s study [14] identified SRSF3 could regulate the production of these functionally distinct HER2 splice variants and therefore maybe important for the regulation of HER2 signaling. The gene discussed is SRSF3; the disease is osteosarcoma.