In lung adenocarcinoma, deletion of HDAC10 accelerates the progression of KRAS-driven cancer both in vivo and in vitro. Specifically, by activating the transforming growth-factor β (TGF-β) pathway, deletion of HDAC10 promotes the expression of sex-determining region Y box protein 9 (SOX9), which subsequently up-regulates the expression of SLUG, as well as CD44. Here, HDAC10 is linked to lung adenocarcinoma.