Unsurprisingly, the reduction in tumour latency was not as great as that observed when a dominant-negative FoxO construct was used to inhibit all FoxOs in the Eμ-myc model.25 Deficiency in a single FoxO does not have an observable effect in all tumour models, however, as loss of FoxO3 or FoxO4 does not accelerate or increase the incidence of DMBA-induced tumorigenesis.25 The gene discussed is FOXO4; the disease is neoplasm.