Given the clinical significance of PTEN, but not the alternative target gene ATAD1 and KLLN (Fig. 6d, e; Additional file 1: Fig. S6b), as well as the evidence of direct interaction between E_156 and the PTEN promoter in melanoma, we evaluated the tumor-suppressive function of E_156 in vitro. The gene discussed is KLLN; the disease is neoplasm.