HPCAL1 and glioblastoma: Besides HPCAL1, other abnormalities of GBM can also stimulate Wnt, including overexpression of Wnt ligand31 and down‐regulation of antagonists of Wnt.29 The function of Wnt and malignant stemness was modulated via the micro‐environment, where agents, such as growth factor of liver cells generated via myofibroblasts, stimulated transcription relying on β‐catenin and promoted cancer stem cell clonogenicity.32 No mutation specific to β‐catenin in GBM has been reported.