It has been reported that TGFβ-mediated apoptosis was suppressed due to the epigenetic silencing of TGFβ type II receptor (TβRII) by high level of EZH2, leading to an up-regulation of ASCL1 in a Smad-dependent manner followed by an accelerated proliferation of SCLC cells in vivo and vitro (29), which is in accordance with the inferior prognosis of ASCL1 positive patients and the significant correlation between ASCL1 and TGFβ1 in our analyses. This evidence concerns the gene EZH2 and small cell lung carcinoma.