Unfortunately, most responses are transient in part due to the development of secondary mutations in NRAS [6], increased expression of the cancer Osaka thyroid (COT, also known as MAP3K8) kinase [7], or more commonly the upregulation of receptor tyrosine kinases (RTKs) like the platelet-derived growth factor receptor beta (PDGFRβ) [6] or the insulin-like growth factor-1 receptor (IGF1R) [8]. This evidence concerns the gene IGF1R and cancer.