MTTP and steatosis: How the HCV genotype 3 virus exerts this cytopathic effect remains to be determined, though previously it has been hypothesized that the greater propensity for development of steatosis, than observed for other HCV genotypes [43], [45], may be secondary to a greater impairment of lipid export from infected hepatocytes [47], [48] possibly mediated by inhibition of microsomal triglyceride transfer protein (MTP) [49], [50] or due to increased availability of free fatty acids by reduced oxidation or by increased de novo synthesis [51], [52], [53], [54] mediated by the HCV genotype 3 core protein.