YBX1 and renal cell carcinoma: To further implicate the functional significance of lncTCFL5-2 and YBX1 interaction in regulating the sensitivity towards Sunitinib, we found that exogenous expression of the wildtype lncTCFL5-2 can partially reverse the reduction of cell viability in response to Sunitinib and THZ1, while mutant lncTCFL5-2 was even lower than the control, suggesting that THZ1 can suppress the lncTCFL5-2 expression likely through suppressing super enhancer [18] activity to resensitize RCC cells to Sunitinib under hypoxia in RCC cells (Fig. 5M).