Our findings suggested that the phosphorylation at Ser 99 and Serine 1107 of TET2 were important for its protein stability, which is different from the conventional phosphorylation-priming for the recruitment of E3 complexes and subsequent proteasome degradation.24 Unlike the recent study demonstrated the YAP/TEAD was activated to counteract apoptosis when treated NSCLC in combination with EGFR and MEK inhibitors,39 we found the Hippo signaling has not been activated in both osimertinib-resistant cells (Supplementary Fig. 12a). The gene discussed is TET2; the disease is non-small cell lung carcinoma.