We conclude that (1) specific AS events and splicing factors are enriched in GBM at recurrence, (2) SRSF5 is upregulated in recurrent GBM and promotes glioma invasion, and (3) many highly tumor-specific AS events are prevalent in the GBM population and are promising candidates for autologous T cell approaches. This evidence concerns the gene SRSF5 and glioblastoma.