STAT1 resides in the cytoplasm before phosphorylation and translocates into the nucleus in order to control the transcription of target genes, such as TARC, MDC, and RANTES. As expected, UT dramatically inhibits the TNF-α/IFN-γ-induced activation of MAPKs and NF-κB/STAT1 in AD-induced HaCaT cells. Here, CCL17 is linked to Alzheimer disease.