reported that EGFR inhibition in lung cancer cells inactivates ETS1 function by reducing AKT activity, and the sustained inactivation of ETS1 reduces the expression of DUSP6, leading to the abnormal activation of ERK1/2 and the induction of TKI resistance.[65] Thus, the specific role and associated mechanism of ETS1 in modulating the sensitivity of ccRCC to TKIs need to be further studied. Here, DUSP6 is linked to nonpapillary renal cell carcinoma.