However, since STAT1-mediated gene regulation within immune effector cells is necessary for mediating the anti-tumor effects of IFN-α [4], the variations in treatment responses seen in these studies may be the result of the varied ability of the administered low-dose IFN-α to activate the Jak-STAT signaling pathway on a patient-by-patient basis. The gene discussed is SOAT1; the disease is neoplasm.