While it requires further validation of TF as a bona fide substrate of CMA, it is interesting to speculate that activation of mTORC2/AKT axis in subsets of EGFR-mut and TKI-resistant NSCLC cells may perturb the physiological balance of CMA activity leading to aberrant accumulation of malignancy-promoting targets such as TF. This evidence concerns the gene AKT1 and non-small cell lung carcinoma.