VIM and neoplasm: In acquired sorafenib resistance, several mechanisms are involved, including PI3K/Akt and JAK-STAT as compensatory pathways, hypoxia-inducible factors, transcription factors such as c-myc, and epithelial to mesenchymal transition factors including vimentin [8], autophagy, microRNAs (such as miR-21; miR-122), tumor microenvironments, or tumor metabolism [9,10].