Single-cell genomic studies have demonstrated that subclonal KRAS and NRAS mutations are often present in distinct clones in other cancer types, and frequent convergence from multiple RAS mutated subclones at diagnosis to a single clonal RAS mutation at relapse has been reported in ALL.24, 31, 32 Considering these data, coexisting subclones of RAS mutations detected in this study likely represent individual subclones, which collectively increase the total mutational burden within a single sample. This evidence concerns the gene NRAS and acute lymphoblastic leukemia.