Interestingly, consistent with our previous hypothesis that de‐methylation was an important mechanism for the reactivation of CT genes in cancers,6 seminomas are also a group of cancers that lack of DNA methylation.10 Thus, the globally de‐methylated genomes of seminoma cells could serve as the epigenetic mechanism for CT genes expression in TGCT.6 However, in contrast to non‐germ cell solid cancer,6 CT genes in TGCT are prone to be expressed in samples with driver genes (KIT, KRAS and NRAS) mutations, which may be attributed to the altered aneuploidy and genomic instability in these samples. Here, NRAS is linked to testicular germ cell tumor.