TCHP and acute myeloid leukemia: Adamia et al. used genome-wide alternative splicing screening in a cohort of AML cells, finding that approximately 29% of them expressed differently spliced oncogenes, tumor suppressor proteins, splicing factors, and proteins involved in apoptosis, cell proliferation, and spliceosome assembly; they concluded that aberrant splicing is a common feature in AML, and that the splice variants may provide novel disease markers and potential targets for small molecules or immune therapies [112].