Our present study shows that T-ALL cells rely on the SKP2/p27Kip1 axis more heavily than normal T-cells for cell growth, and that SKP2 inhibition antagonizes T-cell leukemogenesis while resulting in little toxicity to normal cells, thus providing a proof-of-concept for targeting SKP2 in T-ALL leukemia. The gene discussed is SKP2; the disease is leukemia.