In both cases, treatment with a FLT3 inhibitor-containing therapy reduced clones with FLT3 mutations, however, with a concurrent expansion or selection of other clones frequently involving RAS/MAPK signaling pathway mutations, which is in line with a recent study utilizing the same scDNA-seq platform in gilteritinib-treated AML patients28. The gene discussed is FLT3; the disease is acute myeloid leukemia.