CDKN2A and malignant glioma: Those data might in part reflect the complexity of p53 regulation and influence of cellular context in different type of tumors, but also suggest a new mechanism of action (MOA) of LZAP in human malignant glioma, that is, complex formation between LZAP and ARF might modulate the functionality of HMD2 towards the p53 polyubiquitination and proteasome-mediated degradation.