We identified typical GCT driver events in our cohort, including KRAS substitutions and gains of the KRAS and KIT oncogenes, as well as other drivers such as an AKT1 substitution and a homozygous deletion of the tumour suppressor gene PTPRD (Supplementary Data 4, 5, 7, 8)6,8,11. The gene discussed is KIT; the disease is granular cell tumor.