Such different behavior may suggest that the immunosurveillance mechanisms involving perforin and complement are necessary to counteract the escape of an autochthonous slow-growing Her2+ mammary tumor in the neuT model, where spontaneous antitumor antibodies arise during tumor progression [32], but are not able to induce the rejection of a fast-growing transplantable Her2+ mammary tumor, a model in which no spontaneous humoral response to Her2 is detected [16]. The gene discussed is ERBB2; the disease is neoplasm.