NEAT1 and glioblastoma: More specifically, SRSF1 is known to contribute to GBM pathogenesis by either splicing-dependent mechanisms (e.g., by increasing the ratio of pro- to anti-oncogenic splicing isoforms of myosin IB (MYO1B) [30,31] and MAPK Signal-Integrating Kinase 2 (MKNK2) [32]) or splicing-independent mechanisms (e.g., by stabilizing the oncogenic nuclear paraspeckle assembly transcript 1 (NEAT1) [33] or by a competitive self-binding interaction that inhibits the targeting of its mRNA transcript from mir-505-3p [34]).