Importantly, the pattern of somatic mutations in clonal hematopoiesis preceding acute myeloid leukemia (AML) was distinct from that in benign CHIP, showing more mutations per sample and higher variant allele frequencies, indicating greater clonal expansion and the enrichment of mutations in specific genes resembling CHOP (e.g., TP53 and spliceosome genes like U2AF1) [19,20]. This evidence concerns the gene TP53 and acute myeloid leukemia.