CHM contains several active compounds that interact with target proteins involved in EGFR-TKI resistance (Bing et al., 2018), in addition to enhancing the inhibition effect of EGFR-TKIs in gefitinib-resistant NSCLC cells by activating PI3-K/Akt-mediated suppress of MUC1 expression (Li et al., 2016). This evidence concerns the gene EGFR and non-small cell lung carcinoma.