Hu et al. constructed a coexpression network by calculating the differentially expressed genes (DEGs) between 971 glioma samples and 102 normal samples, and functional and pathway enrichment analyses indicated that the p53 signaling pathway and the pathway of neuroactive ligand-receptor interaction may play important roles in the progression of glioma, and three genes (PUS7, EFR3B and NRCAM) were potential biological agent landmarks [3]. The gene discussed is EFR3B; the disease is central nervous system cancer.