Bi et al. found that loss of the histone deacetylase HDAC11 increased the transcription of LKB1, a serine/threonine kinase, by promoting histone acetylation in the LKB1 promoter region, which activated the AMPK signaling pathway and inhibited the glycolytic pathway, resulting in the inhibition of tumor cell stemness and the improvement of sorafenib resistance (Bi et al., 2021) (Figure 2B). Here, MARK2 is linked to neoplasm.