One explanation for this is that chondroma formation can be initiated by Fgfr3-deficient cells in both mutants, but will be enhanced in mosaic Fgfr3 cKO mice owing to crosstalk between mutant and adjacent wild-type cells, which are not passively incorporated into lesions but may interact with mutant cells to actively promote cartilaginous tumor formation. This evidence concerns the gene FGFR3 and neoplasm.