TSC2 and neoplasm: We show that loss of function of TSC2 in genetic backgrounds that abrogate senescence and proliferation arrest is sufficient to convert mouse and human renal proximal tubular epithelial cells into neoplastic stem cells that give rise to allograft or xenograft tumours that reproduce many of the histological and molecular features of human renal AMLs, providing the first models of AML-like tumours.