Folgiero et al. demonstrated that TIM-3+ NK cells interact with AML blasts expressing Galectin-9 (Gal-9), and inhibition of TIM-3 or Gal-9 affected NK cell-dependent IFN-γ production as well as the activation of IDO1 in AML blasts [18]. The gene discussed is HAVCR2; the disease is acute myeloid leukemia.