Using NGS on AML patients of FLT3‐ITD‐specific subgroup at three different time points, diagnosis, complete remission and relapse revealed that clonal evolution occurred in either two ways – (a) a dominant clone that acquired new somatic aberrations due to DNA damaging therapeutic agents and expanded in relapse or (b) subclones pre‐existing in low numbers at diagnosis evaded killing and prevailed as the dominant clone at relapse [70]. Here, FLT3 is linked to acute myeloid leukemia.