It is well established that stable expression of the oncogenes HPV16 E6 and E7 induces the EMT in cervical cancer cells through a series of mechanisms that ultimately increase the expression of the EMT-activating transcriptional factors Slug, Twist, ZEB1, ZEB2, α-SMA, Vimentin and fibronectin, and reduce the protein expression of E-cadherin through a DNA methyltransferase 1-dependent mechanism [39–42]. Here, ACTA1 is linked to cervical carcinoma.