For example, SP1 facilitated STK39 expression by binding to its promoter and promoted the proliferation, migration, invasion and epithelial-mesenchymal transition of hepatocellular carcinoma cells [25]; SP1 interacted with ZFPM2-AS1 promoter to transcriptionally activate ZFPM2-AS1 expression and aggravated glioma progression [26]. This evidence concerns the gene STK39 and central nervous system cancer.