This innovative design achieves synthetic immunity by using an IL‐2 variant (IL‐2v) that does not bind to CD25, aiming to limit Treg activation while redirecting IL‐2 activity to NK cells via cis‐engagement of NKp46, CD16a and IL‐2Rβ, and by creating a specialised connection between NK and tumour cells, facilitating targeted destruction of the latter. The gene discussed is NCR1; the disease is neoplasm.