Taken together, the above data suggest that inhibition of HDAC8 results in upregulation of NEK1 to increase the phosphorylation of ETS1 at the T241 site, which influences ETS1‐K245ac to enhance the interaction between ETS1 and HIF‐2α and is responsible for acquired drug resistance after sunitinib treatment in ccRCC cells (Figure 6Z). The gene discussed is EPAS1; the disease is nonpapillary renal cell carcinoma.