Furthermore, another murine model-based study clearly demonstrated that the TNF derived from inflammatory liver macrophages is indispensable for NASH and steatohepatitic HCC development under high-fat diet (HFD) feeding conditions in MUP-urokinase plasminogen activator (commonly known as uPA) mice (14); this effect occurs through the transient endoplasmic reticulum (ER) stress response, which enhances lipogenesis and increases the degree of hepatic steatosis (15–17). This evidence concerns the gene PLAU and steatosis.