SLU7 and hematologic disorder: Growing evidence highlights the role of aberrant splicing in various biological processes, including angiogenesis, epithelial‐to‐mesenchymal transition (EMT), and tumorigenesis.[5, 6, 7, 8, 9, 10, 11, 12] While genetic mutations in splicing factors (SFs) have been reported as drivers of splicing dysregulations in hematologic malignancies, increasing evidence suggests that aberrant splicing can persist even in the absence of splicing factor mutations.