HDAC5, another class-IIa HDAC, has been described as a modulator of the inhibitory functions of Foxp3+ regulatory CD4+ T cells (Treg) (24), but inoculation of Hdac5 knockout mice with congenic TC61 lung adeno-carcinoma cells did not result in decreased tumor growth compared to wild type littermates despite a defective immune suppressive capacity of Hdac5-deficient Treg, which can be explained by a simultaneous impairment of IFNγ production in Hdac5-deficient CD8+ T cells (24). The gene discussed is IFNG; the disease is neoplasm.