To further corroborate our results, we analyzed the expression levels of JUNB protein in experimentally induced mouse nucleophosmin-anaplastic-lymphoma-kinase (NPM-ALK) driven T-cell lymphomas [15] being wildtype, hemizygous or negative for JunB. JunB deletion was achieved in T-cells facilitating a CD4 driven CRE and a floxed JunB construct [17]. This evidence concerns the gene NPM1 and T-cell non-Hodgkin lymphoma.