In addition to the well-established reactivation or induction of tumor suppressor genes such as p53, Rb or PTEN [[20], [21], [22], [23], [24], [25]], which is desirable in the context of tumor therapy, this study demonstrates that HDACi can also lead to an unwanted upregulation or activation of well-established (proto-)oncogenes such as EGFR. The gene discussed is TP53; the disease is neoplasm.