In our study, the inhibited apoptosis caused by PAX8-AS1 overexpression in HL60 cells was accompanied by the higher expression of Bcl-2 and the lower expressions of Bax and C Caspase-3, and the promoted apoptosis resulted from PAX8-AS1 silencing in HL60/ADM cells was concurrent with the downregulation of Bcl-2 levels and upregulation of Bax and C Caspase-3, which indicated that PAX8-AS1 could affect the result of AML patients through apoptotic mechanism-mediated drug resistance. Here, BAX is linked to acute myeloid leukemia.