Specifically, the binding of estrogen (E2) to estrogen receptor alpha 36 (ERα 36) significantly promotes the proliferation of laryngeal cancer cells and activates molecules such as protein kinase C (PKC) and phospholipase D. These mechanisms not only enhance the resistance of cancer cells to chemotherapy-induced apoptosis but also promote angiogenesis and tumor metastasis, supplying the tumor with necessary blood and nutrients (34–37). Here, PRRT2 is linked to neoplasm.