For example, although CDK16 was found to be a target of PRMT5 in acute myeloid leukemia,[32] it was not identified in PRMT5‐deleted hematopoietic stem cells.[14b] In PRMT5 inhibitor‐treated glioblastoma stem cells, yet a different set of cell cycle genes showed differential splicing.[31b] These findings suggest that PRMT5‐affected gene splicing is context‐dependent and varies across different tissue types. This evidence concerns the gene PRMT5 and glioblastoma.