These possibilities would be best tested by whole-genome sequencing of a larger cohort, however, we did note that KRAS/BRAF/HRAS/ERBB2/NRAS-wildtype tumours were enriched for loss of heterozygosity on 17q in both the SBT and LGSC cohorts (combined p = 0.005 FET), which is potentially associated with an alternative driver such as NF1 although only a single truncating NF1 mutation was detected in this study. This evidence concerns the gene HRAS and neoplasm.