We pulsed cohorts of Fgfr3-creER; Trp53fl/+; R26RtdTomato (Fgfr3-p53 Control), Fgfr3-creER; Trp53fl/fl; R26RtdTomato (Fgfr3-p53 cKO) at P21 and analyzed these mice at 9 months of age when half of the Fgfr3-p53 cKO mice dropped out from the study due to excessive tumor burden (Fig. 7a). This evidence concerns the gene TP53 and neoplasm.