HDAC11, which is upregulated in the stem-like population of NSCLC, interacts with the transcription factor GLI1 to activate the expression of SOX2. Moreover, selective HDAC11 inhibitors (FT234 and FT895) efficiently inhibit the growth of drug-resistant lung adenocarcinoma stem cells120. Here, HDAC11 is linked to non-small cell lung carcinoma.