T. gondiiis a globally distributed intracellular protozoan parasite affecting approximately 5-90% of human population and causing a variety of so far neglected diseases and clinical entities in both immunocompromised and immunocompetent individuals. Acute infection of the parasite in mice caused a marked reduction in serum butyrylcholinesterase (BChE) activity and liver damage. BChE and AChE are biomarkers of low-grade systemic inflammation and earlier it was suggested that the elevation of these two bioparameters may predict development of type 2 diabetes mellitus and Alzheimer’s disease. Serum BChE activity was found to be also associated with overweight, obesity, body fat distribution parameters, and recently a positive association between T. gondii seropositivity and obesity has been reported. Infection with the parasite was linked with increase in the number of hepatic stellate cells known to play an important role in development of fibrosis and its advancement to cirrhosis.of any etiology. Moreover, several authors suggested that hepatitis with a clinical picture resembling acute viral hepatitis result from T. gondii infection. Abnormalities associated with cryptogenic liver cirrhosis markedly affect acquired immunity of the host and probably participate in triggering and persistence of several autoimmune diseases, especially that anti-T. gondii IgG antibodies have been found in the sera of both patients suffering from these clinical entities and in healthy individuals. Oxidative stress and immunosuppresion due to the infection play an important role in these processes. It should be also noted that mammalian as well as the parasite cells, express two cholesteryl ester-synthesizing enzymes, ACAT1 and ACAT2, which share 44-47% of amino acid homology. ACAT1 is present in various cells and tissues, while ACAT2 expression is restricted to hepatocytes and intestinal mucosal cells. The parasite enzymes TgACAT1 and TgACAT2 localized to endoplasmic reticulum can synthesize and store abundant esters of cholesterol and triglycerides. The lifelong persistence and resulting surplus of ACAT1 and ACAT2, and TgACAT1 and TgACAT2 enzymatic activities especially in the hepatocytes and/or intestinal cells of the host may therefore at least in part be responsible for development of steatohepatitis, and generation of ballooning hepatocytes, foamy macrophages, and clear cells (foamy) colitis. These abnormalities can be explained by the suppressed autophagy in the liver due to proliferation of T. gondii. In alcoholic steatohepatitis, ballooning degeneration of hepatocytes may also at least partly result from the fact that ethanol dose-dependently stimulate microneme secretion in T. gondii tachyzoites and parasite attachment to host cells, thus facilitating infection of the hepatic cells. The increased serum iron levels and hepatic iron overload reported in patients with nonalcoholic hepatitis may be caused by the excess of NO produced by activated macrophages and hepatic cells of the host, as a defense molecule against infection with the parasite. NO intercepts iron before incorporation into ferritin and directly mobilizes iron from the serum protein in a glutathione-dependent manner. Finally, several reports provided data suggesting that the generation of Mallory-Denk bodies is linked with latent chronic hepatic toxoplasmosis, and T. gondii cathepsin L and B proteases play an important role in this process.