KIT mutations predominantly clustered in activating hotspots (exons 11 and 17)23, while KRAS mutations frequently affected activating codons, with G12 (n=15), Q61 (n=5), and A146 (n=3) observed in seminomas, and G12 (n=4), Q61 (n=1), and A146 (n=1) in non-seminomas (Supplementary Fig. 3). Here, KIT is linked to seminoma.