SP4 and cancer: In cancer cells, SRSP is upregulated and increases the recognition and binding of SRSF3 on exon 3 of Sp4 to induce the inclusion of exon 3 to produce the “cancerous” splicing variant L‐Sp4 of the Sp4 gene; in normal cells, SRSP is absent or expressed at a low level so that SRSF3 weakly recognizes and binds to exon 3 of Sp4, thereby resulting in the skipping of exon 3 to produce the “noncancerous” splicing variant S‐Sp4 of the Sp4 gene (Figure 8G).