ERBB2 and neoplasm: Three of six “wildtype” tumours had identifiable alternative RAS/MAPK or ERBB2 pathway mutations–novel ARAF (p.(G11E)) and NCK1 (p.(E336del)) mutations in combination, PAK1 (p.(S57_I58insFFR)) and NF1 (p.(E1119X)) mutations in combination, and an ERBB2 essential acceptor splice site mutation that results in skipping of exon 16 (Supplementary Figure S6A), which encodes part of the growth factor receptor IV domain, in combination with a truncating TSC1 mutation (p.(P141fs11X)).