Non-alcoholic fatty liver disease (NAFLD) is currently the most common liver disease worldwide. It is characterized by aberrant lipid storage in hepatocytes, named hepatic steatosis. While some of them develop into non-alcoholic steatohepatitis with or without fibrosis. The liver can be considered as an “immune organ” because it adjusts non-lymphoid cells, such as macrophage Kupffer cells, stellate and dendritic cells, and lymphoid cells. Many of these cells are components of the classic innate immune system, enabling the liver to play a major role in response to pathogens. Although the liver provides a “tolerogenic” environment, aberrant activation of innate immune signaling may trigger harmful inflammation that contributes to tissue injury, fibrosis, and carcinogenesis. A pivotal role in liver inflammation is also played by cytokines, which can initiate or have a part in immune response, triggering hepatic intracellular signaling pathways. In this review, we discuss the relevant role of innate immune cell and cytokines in relation to NAFLD.