Consistent with these results, ubiquitinated Notch levels were clearly increased in PLK2 overexpressed samples compared with levels in control groups (Fig. 6l and Supplementary Fig. 4 L), indicating that loss of PLK2 stabilized Notch1 through suppressing degradation of Notch1 protein then activated Notch signaling, which finally leaded to acquired TMZ resistance and tumor recurrence. Here, PLK2 is linked to neoplasm.