Thanks to its absence on normal hematopoietic stem cells and its expression on LSC, CLL1 was explored as a marker for minimal residual disease in AML.67 To test the effect of targeting CLL1 in AML, the Fab fragments of anti-CCL1 and anti-CD3 antibodies were site-specifically modified using the unnatural amino acid, p-acetylphenylalanine and then conjugated to generate a bispecific Fab (BiFab). The gene discussed is CCL1; the disease is acute myeloid leukemia.