Since tumor regrowth (after initial response) is a near universal occurrence in xenograft models (reportedly with continued IGF-1R downregulation and maintained p-Akt) [108] and patients treated with single-agent IGF-1R targeted therapies to date, a fresh approach must seek to obviate not only IGF-1R signaling but also the cancer type-specific resistance mechanism(s) as well. Here, IGF1R is linked to cancer.