T-bet suppresses the expression of immature NK cell-defining genes.

RUNX2 plays an important role in human NK cell biology by driving differentiation, inhibiting cytokine production, and inducing a tissue-resident phenotype, which has implications for improving NK cell therapy for cancer patients.

Deficiency of the transcriptional repressor, Bach2, results in more mature mouse natural killer cells.

Multiomic analyses provide new insights into the involvement of transposable elements in T-cell development in the thymus and central tolerance induction.

mTORC1 and mTORC2 play a central role in the development of natural killer (NK) cells.

Neonatal ILC1-like cells are functionally immature but have the unique potential to generate NK cells characterized by downregulation of NKG2A and a highly diverse KIR receptor repertoire.

Chronic engagement of Natural killer cell inhibitory receptors by MHC-I molecules maintains a high activity of the mTOR pathway allowing subsequent amplification of signaling through activating receptors upon acute stimulation.

Interleukin 15-producing microenvironments in the fetal and adult liver foster a type 1 innate lymphoid cell lineage with intrinsic cytotoxicity mediated through cytotoxic granules that are expressed under their steady state, unlike conventional natural killer cells with stimulation-dependent cytotoxicity.

Natural killer cells that were commonly thought to circulate around the body can actually reside in distinct tissues, such as in the liver, skin or uterus, and do not re-circulate.

Antitumor (natural killer) NK cell responses are negatively regulated by interactions between NK cells and endogenous NKG2D ligands constitutively expressed on lymph node endothelial cells and super-induced on tumor-associated endothelium.