EGFR and neoplasm: Secondary resistance can be divided into dominant (ALK intra-kinase domain mutation, increased copy number gain of ALK gene) and non-dominant such as tumor heterogeneity, bypass signaling pathways activation such as the EGFR, Kirsten rat sarcoma viral oncogene homolog (KRAS), v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog (KIT), met proto-oncogene (MET), and insulin-like growth factor 1 receptor (IGF-1R), as presented in Figure 2 [30,31].