Malignant transformation of cervical cancer ensues from failure in the defense against the virus infection, manifesting as interrupted cellular machinery, including DNA replication, inefficient immune response, chronic inflammation (Boccardo et al., 2010), disruption of p53 expression and function (Ruttkay-Nedecky et al., 2013), and abnormal PI3K/AKT/mTOR signaling (Zhang et al., 2015; Bossler et al., 2019). The gene discussed is TP53; the disease is viral infectious disease.