The conversion of effector NK cells (CD49a−CD49b+ Eomes+) was demonstrated into ILC1s including intermediate ILC1 (intILC1) (CD49a+ CD49b+ Eomes+) and ILC1 (CD49a+ CD49b− Eomesint) populations that were not capable of restraining tumor growth and metastasis through TGF-β signaling in the tumor microenvironment (71). This evidence concerns the gene ITGA2 and neoplasm.