Similarly, we found that even though EGFR inhibition potentiated the effect of ALK inhibition in the ALK‐rearranged lung cancer cells, normal lung epithelial cells also showed a generic toxic response to co‐targeting of EGFR, which aligns with severe toxicity in NSCLC patients receiving combinatorial treatments with ALKi and EGFRi [36, 37]. This evidence concerns the gene EGFR and lung carcinoma.