JAK-ing up the Response to KIT Inhibition

Abstract

Only a subset of patients with KIT-mutant melanoma derives clinical benefit from KIT inhibition, and the development of resistance is common. Efforts to improve the efficacy of KIT inhibition are limited by a lack of understanding of the mechanisms underlying response and resistance to treatment. Findings from Delyon et al. suggest that signal transducer and activator of transcription 3 activation may be an important mediator of response to nilotinib.