The delayed cartilage tumor onset and growth and the expanded growth plate cartilage in old SHP2KOBglap mice could be explained by the relatively weak activity of Bglap-Cre, which would prolong the time needed to excise both SHP2-floxed alleles, in contrast to the robust activity of Col2α1-Cre and Ctsk-Cre in cartilage.60,63 The time lag for osteochondroma development could also reflect the time required for mutations in other genes to occur and manifest themselves in benign tumor formation. This evidence concerns the gene COL2A1 and Osteochondroma.