Taken together these results suggest a model wherein NF-Y, in collaboration with E2F4 and/or MYBL2 and FOXM1 complexes, binds to and activates transcription of E2F/NF-Y/CHR dependent switch genes accelerating late phase of cell cycle with a consequent increase of cancer progression and rewiring of some metabolic pathways, hallmarks of the malignant transformation (Fig. 6). The gene discussed is FOXM1; the disease is cancer.