Further studies have revealed that CD44 acts as an ERK-dependent downstream effector of serglycin, which can activate the MAPK/β-catenin axis to induce CD44 receptor expression in nasopharyngeal carcinoma [40]. CD44 can regulate a number of central signaling pathways, including the PI3K/AKT, Rho GTPase, and Ras-MAPK pathways [41]. In our study, we found that Bach1 silencing significantly repressed the MAPK pathway. This evidence concerns the gene AKT1 and nasopharyngeal carcinoma.