In malignant hepatocytes, CD44 overexpression correlates with poor clinical outcomes and facilitates tumor progression by sustaining receptor tyrosine kinase signaling, repressing pro-apoptotic Fas expression, and maintaining cancer stem cell features through crosstalk with epidermal growth factor receptor (EGFR), mesenchymal–epithelial transition factor (c-Met), platelet-derived growth factor receptor beta (PDGFR-β), and TGF-βRI pathways [12,94,95]. The gene discussed is CD44; the disease is neoplasm.