In contrast, tMN without antecedent CH clones were primarily related to dominant TP53 mutations (40%), followed by lesions involving PPM1D (15%), KRAS/NRAS (5%), EZH2/SUZ12 (5%), SF3B1 (5%) and U2AF1 (5%) (Fig. 4B). Here, KRAS is linked to therapy-related myeloid neoplasm.