Therefore, FLCN alteration appears to be a relatively strong tumour driver given the fact that FLCN-deficiency leads to kidney cell proliferation in both in-vivo and in-vitro models, whereas mutation of other kidney cancer-associated genes including VHL and fumarate hydratase (FH) in genetically manipulated murine models only develop renal cysts.6 This evidence concerns the gene FH and neoplasm.