If confirmed in a larger cohort of patients, this difference could let us envision a different preferential mechanism of progression between the two entities: one CHIP-linked (through clone expansion and/or acquisition of additional mutations), more common in NK t-MN, versus correlated to chromosomal destabilization, specific for abnormal karyotype t-MN, characterized by TP53 mutations at the time of first malignancy. This evidence concerns the gene TP53 and therapy-related myeloid neoplasm.