There is a high degree of variability in this response presumably due to inter-individual differences in the size and responsiveness of the residual tumor, the baseline (untreated) levels of serum GH and resulting serum IGF-1, expression of SST2 receptors in the tumor cells, the contribution of the GH receptor toward total IGF-1 secretion from the liver, and other unknown factors [33–35]. Here, IGF1 is linked to neoplasm.