In summary, isopretGO analysis showed downregulation of KRAS4A and upregulation of KRAS4B in both hepatoblastoma datasets; since these isoforms are predicted to have different functional profiles (multiple different GO annotations), one could hypothesize that alternative splicing of these isoforms is associated with the pathobiology of hepatoblastoma (Figure 4). Here, KRAS is linked to hepatoblastoma.