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Understanding resistance to BCL2 inhibition is a critical scientific and clinical challenge. In this issue of Cancer Discovery , two laboratories use unbiased approaches of large loss-of-function CRISPR/Cas 9 screens to discover targetable liabilities in cell signaling and metabolism to acute myeloid leukemia resistant to BCL2 inhibition. See related article by Chen et al., p. 890 . See related article by Nechiporuk et al., p. 910 .

Mitochondrial Homeostasis in AML and Gasping for Response in Resistance to BCL2 Blockade