Using astrocytes derived from conditional STAT3 knockout mice, the authors found that the simultaneous deletion of STAT3 and shRNA knockdown of PTEN resulted in a dramatic increase in cell proliferation in vitro and tumor formation in SCID mice, whereas siRNA knockdown of PTEN alone (i.e., in the presence of normal STAT3 expression) resulted in significantly less tumorigenic effects in these cells. The gene discussed is PTEN; the disease is neoplasm.