In line with these findings, a recent proteogenomic analysis identified the PA2G4-MYC axis as a druggable vulnerability in 3q26-amplified acute myeloid leukemia (AML) [22], where PA2G4 overexpression conferred resistance to HDAC inhibitors, while its inhibition suppressed leukemia progression in patient-derived xenograft models. Here, HDAC9 is linked to acute myeloid leukemia.