A survey of genetic interactions, using the enCas12a multiplex knockout platform, showed major network rewiring between FASTS and other AML cells and revealed strong genetic interactions in FASTS cells with GPAT4, a key enzyme in the processing of saturated fatty acids, and its regulator CHP1. Collectively these observations suggest that FASTS cells are near some critical threshold for saturated fatty acid carrying capacity, which we validated biochemically by treatment with fatty acids and bioinformatically through analysis of CCLE metabolomic profiles. The gene discussed is CHP1; the disease is acute myeloid leukemia.