63 Together, these findings indicate that (i) the sensitivity of tumors to insulin and IGF-1 parallels their response to CR, and (ii) neither the activation status of PI3K−AKT per se nor mutation status of individual genes predicts for the sensitivity of tumors to both growth factors and CR; instead, the metabolic environment of the host (NOD-SCID mice display signs of both type 1 and type 2 diabetes69) and genetic conformity between host and tumor (xenograft/allograft/isograft) seem to have the dominant role. This evidence concerns the gene IGF1 and neoplasm.