Phosphorylation of eIF2α, a downstream effector of the EnR stress response, was increased in human breast cancer cell lines, HCC70 and MCF7, but not MDA-MB-231 after IGF-1R inhibition (Fig. 2e), while total eIF2α was unchanged, suggesting inhibition of IGF signaling activates EnR stress signaling in breast cell lines with low basal EnR stress. This evidence concerns the gene IGF1R and breast carcinoma.