TP53 mutations account for 40% of t-MN cases (44), likely due to t-MN’s association with a myriad of cytotoxic agents (38), while PPM1D gain-of-function mutations account for roughly 20% of non–TP53-mutant t-MN cases (52) and are driven primarily by platinum-based chemotherapies (38, 52–54). Here, PPM1D is linked to therapy-related myeloid neoplasm.