Existing studies underscores that the inhibitory effect of VD on cervical cancer may be mediated through various pathways and factors, including but not limited to the EAG potassium channel, HCCR-1, estrogen and its receptor, p53, pRb, TNF-α, the PI3K/Akt pathway, and the Wnt/β-catenin pathway. This evidence concerns the gene TNF and cervical carcinoma.