Furthermore, ERK and MEK were abnormally stimulated in gliomas and other malignancies,27 and could serve as an upstream event, and is necessary to deactivate GSK3β.17 Previous studies have demonstrated the interaction between ERK2 and HPCAL1.11 Accordingly, our results provided also suggested that the expression of HPCAL1 lead to the activation of ERK, which would deactivate GSK3β, and therefore constrain the activity of β‐catenin. The gene discussed is GSK3B; the disease is central nervous system cancer.