For Ki-67 ≥ 30%, univariate analysis suggested that the presence of nodule-in-nodule architecture (p = 0.069), presence of mosaic architecture (p = 0.060), presence of coronal enhancement (p = 0.045), presence of rim APHE (p = 0.003), presence of delayed central enhancement (p = 0.064), presence of targetoid restriction (p = 0.086), presence of satellite nodules (p = 0.050), presence of portal and hepatic vein tumor thrombus (p = 0.035), and presence of peritumoral enhancement (p = 0.030) were potential differential factors for the prediction of HCC with Ki-67 ≥ 30%. Here, MKI67 is linked to hepatocellular carcinoma.