There was not sufficient tissue obtained in the recurrent tumor biopsy for exome or genomic sequencing to elucidate the mechanism of β-catenin activation in this case, but our previous results have demonstrated that β-catenin pathway activation in melanoma can be driven by activating mutations in CTNNB1 (β-catenin) itself, inactivating mutations in inhibitors of β-catenin such as AXIN1, or over-expression of specific Wnt ligands or Frizzled receptors [16]. This evidence concerns the gene AXIN1 and neoplasm.