The clinical development of linsitinib (OSI-906) and other small-molecule tyrosine kinase inhibitors (TKIs) that competitively block the ATP-binding cleft of IGF-1R and insulin receptor alpha (IR-α) has been abandoned due to dose-limited hyperglycemia, which resulted from undesirable binding to the IR-β isoform responsible for insulin-mediated metabolic signaling [36]. Here, IGF1R is linked to Hyperglycemia.