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. This evidence concerns the gene AKT1 and granular cell tumor.