However, contradictory results were reported that lower JMJD2A intensity was observed in bladder cancer tissue samples, predicting significantly worse overall survival.69 JMJD2A promoted the growth and protein synthesis of gliomas via phosphoinositide-dependent kinase-1 (PDK1)-mediated Akt-mTOR pathway activation.70 Notably, there appeared to be no difference between JMJD2A upregulation or downregulation in the growth of cervical carcinoma.71 These results suggested that JMJD2A might preferentially stimulate the growth of specific tumor types. This evidence concerns the gene KDM4A and glioma.