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To stratify patients for MCL\u20101 inhibitor treatment, we evaluated the sensitivity of 42 primary AML samples to MCL\u20101 inhibitor MIK665 (S64315) and analyzed their molecular profiles. We observed that MIK665\u2010sensitive samples had a more differentiated phenotype, whereas resistant samples displayed higher levels of ABCB1 (MDR1) and the anti\u2010apoptotic protein BCL\u2010XL. Moreover,\n                    <jats:italic>ABCB1<\/jats:italic>\n                    expression had good predictive performance in identifying resistant samples. To induce sensitivity, we treated MIK665\u2010resistant samples with ABCB1 inhibitors elacridar or tariquidar, BCL\u2010XL inhibitor A1331852, or BCL\u20102 inhibitor venetoclax in combination with MIK665. The combination of MIK665 with each of elacridar, tariquidar, or venetoclax effectively eliminated AML blasts compared to the agents alone, while the combination with A1331852 showed limited efficacy for this patient subgroup. 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