In line with previous small studies in older AML patients [13–15], the genetic profile largely differed from that of younger patients, with a predominance of mutations in genes involved in CHIP (ASXL1, TET2, SRSF2, and DNMT3A) (Fig. 1A–C), and of adverse-risk molecular and cytogenetic features accounting for 73% by the 2022 ELN risk classification (Fig. 1A–C, Table 1) [17]. Here, DNMT3A is linked to acute myeloid leukemia.