The tumor suppressor P53 is a transcription factor that activates transcription of a number of target genes to regulate cell cycle arrest, DNA repair, immunity, inflammation, and apoptosis. Our previous study showed that zinc finger CCHC-type containing 10 (ZCCHC10) plays an anti-oncogenic role through activating P53 in lung cancer and acute myeloid leukemia. To further investigate the mechanism of ZCCHC10 in acute myeloid leukemia, transcriptome analysis of ML2 cells overexpressing ZCCHC10 gene or empty vector was performed by RNA sequencing (RNA-seq), and a total of 1 284 differentially expressed genes were iden-tified [|log2(fold change)| ≥1, q value < 0.05], including 778 upregulated genes and 506 downregulated genes. The chemokine CCL18 was significantly upregulated (18-fold) in ZCCHC10-overexpressing ML2 cells. Bioin-formatics analysis revealed that the CCL18 gene promoter contains two P53 response elements. Biotin-labeled DNA affinity assay and chromatin immunoprecipitation (ChIP) assay confirmed the binding of P53 to the CCL18 promoter. Luciferase activity analysis showed that P53 enhanced CCL18 promoter activity. The study sug-gests that ZCCHC10 promotes CCL18 gene expression through activating P53.