Immune “checkpoint” inhibitor antibodies have revolutionized cancer therapy by reactivating tumour-resident cytotoxic lymphocytes. More recently, immune checkpoint therapy is emerging for its potential in restoring immunity against infectious agents. Checkpoint inhibitors primarily block inhibitory pathways in tumour-resident T cells, however interest in other effector populations, such as natural killer (NK) cells, is growing. NK cells are key to cancer immunosurveillance, particularly in settings of metastasis, yet their potential for controlling bacterial infection is less clear. NK cells are dependent on the cytokine interleukin (IL)-15 for their survival, development, and function, but how this cytokine is regulated remains enigmatic. The suppressor of cytokine signalling (SOCS) protein cytokine-inducible SH2-containing protein (CIS, encoded by Cish) is induced by IL-15 and was described as a potent intracellular NK cell checkpoint that suppresses IL-15 receptor signalling. In addition, we have previously discovered that tumours can neutralize NK cell metabolism, proliferation, and activation by the TGF-β immunosuppressive pathway by inducing plasticity of NK cells and differentiation into innate lymphoid cell (ILC)1-like subsets. Here, we investigate whether enhancement of NK cell function can improve anti-bacterial immunity. We identified for the first time NK cell to ILC1-like plasticity within a bacterial infection model, however the precise driver of plasticity is this model remains unexpectedly elusive. We further describe that NK cells from Cish-deficient mice displayed enhanced pro-inflammatory function and dramatically enhanced anti-infection immunity. However, a Cish- and Tgfbr2-double-deficient NK cell mouse model did not synergize for increased resistance to Salmonella infection.