To complicate matters further, activated cNK cells have been shown to downregulate Eomes expression and upregulate ILC1 markers (32–34), resulting in increasingly blurred boundaries between the cell types under inflammatory conditions—for example, NK cells have recently been shown to be able to transition towards an ILC1-like phenotype (Eomes- CD49a+ Ly6C+) as a consequence of IL-12 s following infection with Toxoplasma gondii (32), or in response to TGF-β signaling in the tumor microenvironment (35), in a manner which may be mediated via STAT4 signaling (36). This evidence concerns the gene EOMES and infection.