The ligands of IR, insulin and IGF2, induced the phosphorylation of IR and Akt in HCC cells, and stable overexpression of IR-A in an HCC cell line promoted migration and invasion, tumour growth, tumorigenicity and expression of stemness markers (CD133, CD44).34 These indicate that IR-A is a functional surface molecule to promote cancer stemness of HCC. The gene discussed is PROM1; the disease is neoplasm.