It is hypothesized that continued ribosome stress in SDS HSPCs carrying a heterozygous TP53 mutation selects for clones that inactivate the second TP53 allele and lead to the development of TP53-mutated CH, but also to its progression to myeloid malignancy (Fig. 1b) [1]. The gene discussed is TP53; the disease is cyclic hematopoiesis.