ATG4D and non-small cell lung carcinoma: Taken together, our findings demonstrated that over-repression of miR-101-3p enhanced cisplatin sensitivity by inhibiting cell viability and increasing cell apoptosis, inducing autophagy in NSCLC cells, and the potential mechanism was related with regulating of ATG4D expression, suggesting that the miR-101a-3p-ATG4D axis may become a novel prognostic and therapeutic target for overcoming cisplatin resistance in NSCLC.