It has been forecast that non-alcoholic steatohepatitis (NASH) will have become a leading indication for liver transplants by the end of the coming decade. NAFLD is a hepatic manifestation of metabolic syndrome. Metabolic syndrome, insulin resistance and an ensuing state of lipotoxicity result in hepatocyte damage, which can in turn progress to steatosis and necrosis of hepatocytes, and further, to NASH, fibrosis and cirrhosis of the liver. Numerous cell types are involved in the pathogenesis of NASH. Damaged hepatocytes signal to the cells of innate immunity- mainly Kupffer cells, resident liver macrophages, which assume a pro-inflammatory M1 phenotype, initiating the process of inflammation. In latter stages of the disease there is a polaristion of macrophages towards a profibrogenic M2 phenotype, which activates hepatic stellate cells (HSC), which in turn secrete collagen, representing the proximal cause of fibrosis. The complex role of NK cells in the development of NASH is reflected in the fact that they take part in both initiating inflammation (via secretion of M1-polarising IFN), as well as in limiting fibrosis via killing of activated HSCs. Shedding light on the role that activating NK receptors (namely NKG2D and NCR) play in the development of fibrosis has been the key motivator of this thesis. Utilising a mouse model of NAFLD, steatosis steatohepatitis diet (SSD) feeding, which faithfully replicates some key features of NAFLD, along with genetic knock-out mice (NKG2D-/- and NCRgfp/gfp, respectively), I demonstrated that disease progression is significantly modified in their absence. Aside from a histopatologically determined reduction of fibrosis (which was most pronounced in NKG2D-/- mice), a flow cytometric analysis has determined profound alterations in certain immune cell populations (namely, macrophages, Treg cells,  T cells and NK cells). The significance of these changes needs to be elucidated further.