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This article has been peer reviewed. It is the authors' final version prior to publication in The Journal of investigative dermatology.

Volume 133, Issue 8, August 2013, Pages 1928-9.

The published version is available at DOI: 10.1038/jid.2013.136. Copyright © Nature


Despite recent advancements in the treatment of late-stage mutant BRAF (V600E/K) melanomas, a major hurdle continues to be acquired resistance to BRAF inhibitors such as vemurafenib. The mechanisms for resistance have proven to be heterogeneous, emphasizing the need to use broad therapeutic approaches. In this issue, the study "Stat3-targeted therapies overcome the acquired resistance to vemurafenib in melanomas" by Liu et al. proposes that signal transducer and activator of transcription 3 (STAT3)-paired box 3 (PAX3) signaling may be a mechanism that is used by melanomas to resist RAF inhibitors.

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