Although the result for unphosphorylated β-catenin was not significant, its elevated expression in glioblastoma indicates the pathway’s activity and its association with genetic changes in APC. The relatively rare expression of β-catenin in the nucleus may also be explained by work from Morgan et al. [78], where they showed that APC loss alone was insufficient to stimulate nuclear β-catenin translocation, and further dysregulation is required. Here, APC is linked to glioblastoma.