H19 was upregulated in erlotinib-resistant NSCLC cells, and the knockdown of H19 could effectively decrease the resistance of erlotinib in cell viability and IC50. Moreover, H19 could be transferred through incorporation into exosomes in erlotinib-resistant NSCLC cells and then induce the resistance of erlotinib by the miR-615-3p/ATG7 axis. Here, ATG7 is linked to non-small cell lung carcinoma.