The growth and survival of tumors do not only depend on one receptor or one signaling pathway, and the drawbacks such as tumor resistance to single-target inhibitors have become increasingly apparent in clinical studies, while the multi-target inhibitor PYR26 can block both c-Met and EGFR signaling pathways, simplifying the treatment process and promising to achieve a single molecule that both inhibits c-Met kinase and restores EGFR at the same time in T790M mutant cancer cells alongside EGFR TK inhibitors, thus overcoming the problem of drug resistance [28,29]. This evidence concerns the gene MET and cancer.