To support this, corresponding clinicopathological analysis of HCC specimens compared to the normal tissue controls revealed that PRSS3-V1 and -V2 were main functional components of clinical relevance since PRSS3-V1 and -V2 were bipolarly present in either PRSS3Low or PRSS3High tissues; therefore, their abnormal coexpression could result in functional heterogeneity including insignificant or paradoxical clinical associations. This evidence concerns the gene PRSS3 and hepatocellular carcinoma.