The controversy is reflected in the potential tumor-suppress role of MEIS1 in prostate cancer30 and clear cell renal cell carcinoma31 and that depletion of MEIS1 as well as MEIS2 enhanced tumor growth by upregulating c-MYC and CD142,7 but the oncogenic role of MEIS1 in glioma.32,33 Therefore, the functions of MEIS1 in different solid tumors need to be further elaborated. The gene discussed is MYC; the disease is central nervous system cancer.