We postulated that if LKB1 deletion indeed induces the osteogenic tumor–like phenotype via activation of the mTORC1 pathway, the deletion of Raptor (the core binding factor of mTORC1) in vivo should lead to amelioration of the osteogenic tumor–like phenotype in Lkb1fl/fl; Ctsk-CKO mice. This evidence concerns the gene CTSK and neoplasm.