The　aim　of　this　study　is　to　estimate　the　role　of　JAK/STAT3　signaling　pathway　on　apoptosis　of　lung　adenocarcinoma　induced　by　icotinib.EGFR　mutation　was　detected　in　lung　adenocarcinoma　cell　line　PC-9　by　ARMS　assay;　The　inhibitory　rates　of　cell　proliferation　of　PC-9　cells　which　were　exposed　to　different　concentrations　of　icotinib　(0~100　μMol/L)　for　different　time　(24~72　h)　respectively　were　evaluated　by　MTT　assay;　Apoptosis　of　PC-9　cells　exposed　to　different　concentrations　of　icotinib　(0,　0.1,　1　and　10　μMol/L)　for　48　h　were　evaluated　by　TUNEL　assay;　JAK2,　STAT3,　Bcl-2,　Bax　mRNA　expressions　were　evaluated　by　Real-time　PCR　assay;　The　protein　levels　of　P-STAT3　and　IL-6　were　evaluated　by　Western-blot　assay.Human　lung　adenocarcinoma　cell　line　PC-9　had　an　exon　19　deletion　mutation　in　EGFR　gene;　Followed　by　treatment　of　icotinib,　the　proliferation　of　PC-9　cells　were　all　inhibited　significantly,　especially　in　48　and　72　h　(P＜0.01)　in　all　concentrations;　The　inhibitory　rates　of　cell　proliferation　in　different　treating　time　had　statistical　significance　(P＜0.01);　Cell　apoptosis　in　different　concentrations　were　increased　significantly　(P＜0.05);　Along　with　the　increasing　concentrations,　gene　expression　levels　of　JAK2,　STAT3　and　Bcl-2　decreased　significantly　(P＜0.05),　Bax　increased　significantly　(P＜0.05),　JAK2/STAT3　ratios　increased　significantly　(P＜0.01),　and　Bcl-2/bax　ratios　decreased　significantly　(P＜0.01);　P-STAT3　and　IL-6　protein　levels　were　inhibited　significantly　in　higher　concentration.JAK/STAT3　signaling　pathway　participates　in　apoptosis　of　PC-9　cells　induced　by　icotinib.　The　most　likely　mechanism　is　icotinib　inhibited　the　gene　expression　levels　of　JAK2,　STAT3　and　Bcl-2,　so　with　the　P-STAT3　and　IL-6　protein　levels,　and　mediated　gene　Bax　overexpression.