TP53 and myelodysplastic syndrome: This is a key observation that pointed towards two important facts: (i) the role of CK1α in AML LSCs regulation is complex but likely more connected to p53 pathway than to Wnt/β-catenin pathway, a known driver of AML [119] that is inhibited by CK1α and (ii) the active p53 signaling is a prerequisite for therapeutic targeting of AML/MDS cells by CK1α inhibition.