A recent study showed that treatment with lenalidomide but not pomalidomide leads to expansion of pre-leukemic Trp53-mutant hematopoietic stem and progenitor cells (HSPCs) due to selective degradation of Ck1α, which offers a potential alternative strategy to mitigate the risk of therapy-related myeloid neoplasms (t-MNs) development (171). The gene discussed is CSNK1A1; the disease is myeloid neoplasm.