To determine whether LSD1 inhibitors provide a new therapeutic concept for treatment of LUAD, six NSCLC cell lines, which harbor different tumor‐driving genetic alterations such as the common KRAS mutations on codon 12 or 61, the activating EGFR deletion in exon 19 or point mutation in exon 21, as well as two different versions of EML4/ALK translocations, were used for cell growth studies. The gene discussed is EGFR; the disease is neoplasm.