While PDGFRA and KDR are co-amplified, KIT is considered the driver oncogene at this locus as it is recurrently mutated in mucosal melanomas.21 The frequent co-occurrence of KIT activating mutations or amplification with NF1 or SPRED1 inactivation has led to the suggestion of using combination inhibitors of KIT and MEK for tumors driven by these alterations.24,25. Here, NF1 is linked to mucositis.