Muts associated with CH are persistent at remission. (A) Bar plot depicting the percentage of muts identified in diagnosis that were also identified at CR1. Numbers to the right of each bar indicate the proportion of variants initially found at diagnosis that were subsequently detected at CR1. Genes are grouped into their relevant biological categories as follows: DNA damage (TP53, ATM); DTAI (DNMT3A, TET2, ASXL1, IDH2, and IDH1); splicing (SRSF2, U2AF1, and ZRSR2); PRC/RUNX (BCOR, BCORL1, RUNX1, and EZH2); cohesin (SMC1A, RAD21, and STAG2); and signaling (CSF1R, FLT3, NF1, KRAS, NRAS, BRAF, KIT, PTPN11, JAK2, CSF3R, and CBL). (B) As in panel A, but individual genes are shown. (C) Violin plot of VAFs for persistent variants at CR1. (D-F) Scatterplot detailing patient-matched VAFs at diagnosis (x-axis) and CR1 (y-axis) for (D) IDH1 and IDH2; (E) DNMT3A, TET2, and ASXL1; and (F) FLT3, NPM1, and NRAS. Each point represents 1 variant in a specific patient, matched across time. DTAI, DNMT3A, TET2, ASXL1, IDH1/2; PRC, polycomb repressive complex.