慢性搔癢會嚴重影響病人身心健康及生活品質，對於健康保險支出，亦是沉重的負擔。傳統上較常使用口服抗組織胺和類固醇等藥物，但療效有限。另外，根據癢的致病機轉，亦有神經傳導物質相關的藥物被證實有效。然而，這些治療並無法完全解決病人慢性搔癢的問題。近年由於異位性皮膚炎的研究，我們對於皮膚屏障破壞到癢的產生機轉，也日益清楚。因此，藉由針對抑制特定細胞激素包括IL-4、IL-13及IL-31等的生物製劑，被陸續研發出來，用以治療異位型皮膚炎及結節性癢疹（一種極度搔癢的皮膚疾病）。此外，由於多種細胞激素的作用，皆須經由JAK-STAT的路徑往下游傳輸，因此近期已有多種抑制JAKs的口服小分子藥物，在臨床試驗和真實世界患者使用中，被證實能有效且快速改善搔癢的嚴重程度。藉由更加了解與搔癢有關的信號傳遞通路，並針對的特定分子予以調控，將可幫助患者在未來擺脫搔癢的噩夢。

"Itching" has negative impact on not only patient's health but also quality of life. In addition, it is a heavy burden on our community resource. Traditionally, antihistamines and steroids are used to control pruritus. In addition, some different mechanisms of medicine, including variety of neurotransmitters are proved to be effective in itching reduction. However, in most of the time the efficacy of these drugs is limited, especially for chronic itching. In recent years, researches on atopic dermatitis (AD) find out the mechanism of damage of keratinocytes and the cause of itchiness. Based on this scenario of pruritus molecular mechanism, several biologics, targeting on interleukin 4 (IL-4), IL-31, IL-31, etc. were developed to control AD and prurigo nodularis, an extremely itching skin disease. Going downstream of the pathogenesis of itching, all the involved cytokines belong to type II inflammation, all of which are activated by the JAK-STAT pathway. A variety of oral small-molecule drugs that inhibit JAKs have been approved to be effectively and rapidly improve the severity of itching in clinical trials and real-world patient usage. Understating the signaling pathway involved in pruritus more and targeting the specific molecules identified allow physicians to help patients get rid of the nightmare of itching in the future.