Regarding the axis of CD226 and TIGIT/CD96/PVRIG, in which shared ligands and receptor-ligand affinities regulate the immune response, it was recently reported that the stimulatory receptor CD226 is downregulated on NK cells from AML patients, whereas in line with our data, an increased expression of TIGIT on T cells and NK cells was observed [19,46]. The gene discussed is CD96; the disease is acute myeloid leukemia.