In studies related to NSCLC, miR-210 was demonstrated to be highly expressed in CAFs-exo and promoted the EMT process in NSCLC cells by down-regulating UPF1 and PTEN, as well as activating the PI3K/AKT pathway thus promoting the EMT process in NSCLC cells (EMT refers to the loss of its epithelial properties by epithelial cells and the adoption of a mesenchymal-like phenotype, and a number of studies have been conducted to confirm that EMT is a tumor metastatic key link) (32). The gene discussed is AKT1; the disease is neoplasm.