The fact that reduction of anti-apoptosis proteins (cIAP-2 or XIAP) by treating head and neck cancer cells with specific inhibitory siRNAs (e.g., cIAP-2 siRNA or XIAP siRNA) during HA/CD44 interaction appears to increase chemosensitivity suggests that downregulation of lncRNA UCA1 together with blockage of survival protein pathways may provide a new therapeutic strategy in cancer therapy, especially dealing with drug resistance. The gene discussed is CD44; the disease is head and neck cancer.