PARP1 had a high connectivity, namely as a basic core, and directly attracted with typical oncogene EGFR and ALK; mutating EGFR in NSCLC constitutively activated encoding protein and caused the occurrence of abnormal function and constant signal transduction out of control, which was in correction with NSCLC development [5]; as a representative molecularly targeted agent, ALK inhibitor could activate recombination through mutation, gene amplification and chromosome abnormality to increase carcinogenic driver expression [6]. This evidence concerns the gene EGFR and non-small cell lung carcinoma.