The hepatitis B virus X protein (HBx) and surface antigen (HBsAg) enhance Liver-CSC stemness and tumorigenicity by upregulating core pluripotency factors (c-MYC, KLF4, NANOG, OCT4, SOX2), surface markers (CD90, CD117, CD133), and dysregulating oncogenic miRNAs through upregulation of miR-181 and downregulation of tumor-suppressive miR-203a (492, 493). The gene discussed is PROM1; the disease is neoplasm.