Several mechanisms are implicated in the reduction of tumor cell sensitivity to sorafenib, such as loops of the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) and janus tyrosine kinase (JAK)/signal transducer and activator of transcription (STAT) pathways, epithelial–mesenchymal transition (EMT) or hypoxia-inducible response5,8,18,19. Here, AKT1 is linked to neoplasm.