Several processes might contribute to the development of therapy-related myeloid neoplasms, including therapy-induced increases in genomic instability with subsequent accumulation of aberrations [221] and the selection of a founder population of hematopoietic stem cells with predisposing clonal hematopoiesis (CH) mutations, such as TP53 mutations [219,222]. This evidence concerns the gene TP53 and myeloid neoplasm.