Supportively, a previous finding showed that RBFOX2 could promote cellular invasion through regulating alternative splicing driven by epithelial–mesenchymal transition.[23] Furthermore, we note that RBFOX2 and the long GOLIM4 variant share similar pro‐tumorigenic functions on NPC cells and the tumor suppressive function of RBFOX2 knockdown could be partially rescued by overexpression of GOLIM4‐L. This evidence concerns the gene RBFOX2 and neoplasm.