To further verify whether the stimulation of ox-LDL-induced hepatic cholesterol disorders was due to the activation of STAT3, we used small interfering RNA (siRNA) to knock down the expression of STAT3; resulting in relieved cholesterol accumulation (Figure 2D), while the overexpression of the STAT3 plasmid aggravated excessive cholesterol accumulation (Figure 2E). This evidence concerns the gene STAT3 and hepatitis A virus infection.