Mechanistically, our validation focused on core genes EXOSC2 and NSUN5: qRT-PCR and Western blot validated significant EXOSC2 overexpression in AML (aligning with its SHAP risk contribution), while NSUN5—despite being a risk factor—showed paradoxical downregulation, suggesting potential post-transcriptional regulation. This evidence concerns the gene NSUN5 and acute myeloid leukemia.