TP53 and cyclic hematopoiesis: It has been reported that the presence, number, persistence, and allele abundance of somatic TP53 mutations were not predictive of leukemia risk in SDS patients with CH, yet, the progression of TP53-mutated clones was found to be driven by the development of bi-allelic alterations of the TP53 locus via deletion, copy number (CN)-LOH, or point mutation (Fig. 1b) [56].