Also, in the functional study by Gao et al., while SALL4 interacts with the HDAC complex, and silences PTEN promoter via reduced acetylation of histone H3 at its binding sites, the SALL4-derived peptide blocks this interaction and leads to reactivated PTEN expression, which induces leukemia cell death that can be rescued by a PTEN-specific inhibitor [64, 96]. The gene discussed is PTEN; the disease is leukemia.