This potential is highlighted by studies demonstrating that PTPN2 deletion in T-cell acute lymphoblastic leukemias in humans is associated with oncogenic JAK/STAT signaling68, whereas in mice the deletion of PTPN2 can also promote STAT-3 signaling to facilitate the development of hepatocellular carcinomas33 or skin carcinogenesis69. The gene discussed is SOAT1; the disease is T-cell acute lymphoblastic leukemia.