We did the function validation in Fig. 9 - using overexpression of CCDC32/CBX3 fusion gene in MV4–11 AML cells for the functional validation with experimental evidence to demonstrate the biological impact of the CCDC32/CBX3 fusion on AML pathogenesis or treatment resistance mechanism by which CCDC32/CBX fusion protein promotes the cell cycle progression with patient-specific MV4–11 Cell Line (FLT3-Mutated AML) (Fig. 9); 3) they did not do patients but We did it to show novelty in AML patients. The gene discussed is CCDC32; the disease is acute myeloid leukemia.