Association between somatic mutations and complete CHR on serial sampling. (A-B) Molecular response among patients allocated to IFNα at baseline (Pre) and at 24 months (Post) of treatment by complete CHR. (A) Among JAK2-mutated patients, those attaining CHR at 24 months had a greater reduction in the JAK2 VAF (median, 0.29 to 0.07; P < .0001) compared with JAK2-mutated patients who did not achieve CHR (median, 0.27 to 0.14; P < .0001). (B) The CALR VAF did not significantly decline among patients achieving CHR nor among those not achieving CHR at 24 months. The middle horizontal lines indicate the median value; box limits indicate the 5th and 95th percentiles, and whiskers indicate the range. All observations are represented by a dot. (C) Number of patients with no treatment-emergent mutations. Significantly more patients with no treatment-emergent mutations treated with IFNα achieved CHR (35 of 68 [51%]) compared with patients treated with HU (4 of 18 [22%]) (P = .03). (D) Number of patients with treatment-emergent mutations. No difference in the number of patients failing to achieve CHR was observed between patients treated with HU (10 of 13 [77%]) or IFNα (9 of 14 [64%]) (P = .68). (E) Number of patients with treatment-emergent DNMT3A mutations. (F) Number of patients with treatment-emergent non-DNMT3A mutations. Treatment-emergent DNMT3A mutations were significantly enriched in patients treated with IFNα failing to achieve CHR (8 of 9 [89%]) compared with treatment-emergent non-DNMT3A mutations (1 of 5 [20%]) (P = .02).