The fact that PPM1D mutants do not completely phenocopy TP53 mutations—for example, PPM1D-mutated t-AML/t-MDS patients do not appear to have the number of chromosomal abnormalities that TP53 mutant t-MDS patients do (Lindsley et al., 2017)—suggests the mechanism may be more complex. The gene discussed is TP53; the disease is myelodysplastic syndrome.