Although Inpp4b deficiency did not cooperate with overexpression H-RasV12, nor E1A, we did observe that Inpp4b deficiency can increase the transformation potential of SV40-T-large transduction suggesting that Inpp4b may function in a tumour suppressive manner in this context, at least in part through its control of Akt activation. The gene discussed is AKT1; the disease is neoplasm.