For other disease-associated genes, including NPM-ALK [28, 29], Rho [30], Dnmt3a [31], STAT3 [32], Myc [33, 34], Akt [35], Maf, [21], Notch [36], Bmi1 [37] and Bcl-2 [38], it has been difficult to address their specific roles in PTCL development; as mice with genetic alterations involving these genes, again with prolonged lag times, frequently develop other hematologic malignancies, often of immature T cell origin, thereby masking their potential contribution to transformation of mature T cells. This evidence concerns the gene MAF and mature T-cell and NK-cell non-Hodgkin lymphoma.