Since most hematologic cancer cells are NMT2-deficient, we originally hypothesized that by targeting the remaining NMT1 in NMT2-deficient hematologic cells, PCLX-001 could selectively kill these cells in a manner reminiscent of synthetic lethality [24], thereby sparing normal human cells with two functional NMTs. This evidence concerns the gene NMT1 and hematopoietic and lymphoid cell neoplasm.