The in-situ tumor model experiments showed that overexpression of MYBL1 significantly abolished its anti-tumor effect on tumor growth of HCC cells treatment with sorafenib, as evidenced by rapid tumor progression, and lower proportions of TUNEL+ and higher proportions of Ki67+ cells, however, inhibition of MYBL1 has the opposite effect (Fig. 8A). This evidence concerns the gene MKI67 and neoplasm.