Examples of CpG hypermethylation targets in cervical cancer cells include, silencing of tumor suppressor BRCA1, DNA-repair enzyme MGMT, mismatch repair enzymes (MLHs) etc. The progression of cervical cancer to more invasive phenotypes is also driven by hyperstimulation of WNT signaling due to hyper-methylation linked repression of a secreted WNT antagonist DICKKOPF-1 in cervical carcinoma cell lines [241]. This evidence concerns the gene MGMT and cervical cancer.