Peptide mimetics of the IGF1R and integrin docking site in Sdc1 (collectively called “synstatin-IGF1R” or “SSTNIGF1R”) inactivate IGF1R and the integrins in breast carcinoma, myeloma, and activated endothelial cells, disrupting cell growth and migration, activating apoptosis by reversing the suppression of apoptosis signal-regulating kinase-1 (ASK1) that occurs downstream of active IGF1R, and blocking tumor growth and tumor-induced angiogenesis in animal models (refs. 17–19; reviewed in ref. 28). The gene discussed is MAP3K5; the disease is plasma cell myeloma.