HDAC is increasingly recognized as a major factor contributing to pathogenesis of cancer including NSCLC.35 Recently, it was reported that the HDAC1, a dominant subtype of HDAC, interacts with TRIB1 to suppress p53 transcriptional activity by enhancing deacetylation and decreasing DNA binding.25 Meanwhile, our previous results indicate that HDAC1 is involved into paclitaxel resistance in NSCLC.22 Therefore, we hypothesis that TRIB1 cooperated with HDAC1 mediate CDDP-enriched CSC. This evidence concerns the gene TP53 and non-small cell lung carcinoma.