Abstract
<h3>Introduction</h3> BCL-2 inhibition has transformed the therapeutic landscape of acute myeloid leukemia (AML). However, 10–50% of newly diagnosed patients with AML may not respond to venetoclax and HMA or LDAC, and 3–15% patients may not respond to venetoclax with intensive or non-intensive chemotherapy.<sup>1–6</sup> In addition, up to 40% of responding patients may relapse with low rates of response of 20% to salvage therapy and poor overall survival of 2 months after relapse.<sup>7</sup> Clinical and biological factors associated with primary and acquired resistance to venetoclax include secondary AML, monocytic differentiation, complex cytogenetics, mutations in TP53, BAX, dependence on other anti-apoptotic proteins, altered metabolism of nicotinamide, fatty acids, and oxidative phosphortylation.<sup>3,8–14</sup>
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