LUC7L2 is involved in chordoma cell survival through alternative splicing and is a potential treatment target.[11] In myeloid neoplasms, LUC7L2 deficiency results in the significant upregulation of the expression of multiple spliceosomal factors and possibly contributes to pathogenesis.[12] LUC7L2 is involved in the regulation of immune infiltration in malignant mesothelioma through alternative splicing.[13] However, whether LUC7L2 participates in GBM TMZ resistance has not been reported, and further study is crucially required. Here, LUC7L2 is linked to myeloid neoplasm.