SRSP, through SRSF3, induces the inclusion of exon 3 of Sp4 to produce the “cancerous” L‐Sp4 isoform containing the transactivation domain in cancer cells; in the absence of SRSP, exon 3 of Sp4 is skipped in normal cells to produce the S‐Sp4 isoform without the transactivation domain and oncogenic features. This evidence concerns the gene SP4 and cancer.