To further investigate the underlying mechanisms leading to PARD3 overexpression in HCC tissues, we first investigated the epigenetics alternations of PARD3 in the TCGA-LIHC dataset by virtue of DNMIVD database [35], yet we didn’t observe any significant changes in the DNA methylation on the promoter region between normal and tumour groups, suggesting that the dysregulation of PARD3 may be not attributed to this epigenetic mechanism (Fig. S9A). The gene discussed is PARD3; the disease is neoplasm.