SP1 and prostate cancer: Overexpression of FABP5 in prostate cancer cells can be attributed to hypomethylation of the CpG island in its promoter region, along with upregulation of the direct trans-acting factors SP1 and c-MYC.9 Hypoxia downregulated the expression of miR-144-3p, which subsequently increased the expression of FABP5 in cervical cancer.13 The different regulatory networks and molecular mechanisms of FABP5 in numerous other cancers still require further study.