For example, EGFR mutants in NSCLC exhibit constitutive internalization and are resistant to degradation due to impaired interaction with E3 ubiquitin ligase CBL, thus leading to prolonged oncogenic signaling.[34, 35] In the present study, we found that CMTM6 is physically associated and co‐localized with EGFR mutants at the cell membrane and in recycling endosomes that are marked by RAB11, thereby promoting lysosome‐mediated degradation of EGFR. The gene discussed is RAB11A; the disease is non-small cell lung carcinoma.