Because of the gain-of-function conferred by the particular mutation within the signal transduction pathway involving FGFR3 and HRAS, mutant spermatogonial cells are proposed to become progressively enriched in the testis over time through a selective proliferation of mutant spermatogonia, leading to clonal expansion which results in the formation of SS tumours in some extreme cases [8]. This evidence concerns the gene HRAS and synovial sarcoma.