EGFR and cervical squamous intraepithelial neoplasia: Additionally, EGFR signaling and the levels of phospho-extracellular signal-regulated kinase 1/2 (p-ERK1/2), a downstream effector of RTKs via the mitogen-activated protein kinase kinase (MEK), increase during cervical intraepithelial neoplasia (CIN) progression from LSIL to HSIL [29–31].