A study conducted by Bures et al suggested that PSCCE exhibits molecular alterations involving the pRB-cyclin D1-CDK4/6-p16 pathway and pTEN.[9] Compared with type I endometrial carcinoma, PSCCE has a unique pathogenesis.[9] No evidence of squamous metaplasia, atypical hyperplasia, or HPV infection was found in our patient, and no cancer was found in the mucosa or stroma of the cervical canal. This evidence concerns the gene CDK4 and endometrial carcinoma.