Most of our CTCL cases with monoallelic breakpoints thus did not exhibit a second hit that could explain silencing of DUSP22. A growing number of tumor suppressor genes are reported to be haploinsufficient, as heterozygous alterations leading to a 50% reduction in gene function are enough to promote oncogenesis [43]. Here, DUSP22 is linked to primary cutaneous T-cell non-Hodgkin lymphoma.