TP53 and glioblastoma: This response is tightly correlated with the nullification, dysfunction, or significant downregulation of the master tumor suppressor gene P53.[41] A study suggested a role for H19 in contributing to GBM malignancy differentiation and the maintenance of its stem cell properties.[42] HOTAIR has been involved in the evolution of several primary tumors, wherein the increase in HOTAIR expression endorses invasion and metastasis.[43] Pastori et al[44] demonstrated that HOTAIR is overexpressed in GBM and controls GBM cell proliferation.