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. This evidence concerns the gene SP1 and cervical cancer.