In particular, EGFR-TKI-resistant cell-secreted lactic acid is swallowed by cancer-related fibroblasts (CAFs), triggering the excess secretion of hepatocyte growth factor (HGF) and subsequent MET signal activation, indicating that there is a non-cellular autonomous metabolic EGFR-TkI drug resistance mechanism (Zhao et al., 2019). This evidence concerns the gene MET and cancer.