Gutbrodt et al. demonstrated that the remodeled BM vasculature in AML can be targeted with mAbs against tenascin C. A fusion protein of anti-tenascin C and IL-2 (F16-IL2) was effective in recruiting CTLs and NK cells to the tumor site and in combination with low-dose cytarabine contributed to tumor clearance in mouse models and patients (176, 177). Here, IL2 is linked to acute myeloid leukemia.