Other trials have supported the strategy of blocking mTOR/p70S6K as a method to control insulin action and potentially avoid upregulation of IGF-1R signaling by inhibition of mTOR.91 While preclinical data support the concept that mTOR inhibition can overcome insulin stimulation of breast cancer,92 the combination of anti-IGF-1R with mTOR inhibitors (Table 1) to suppress further signaling93 has proven to be too toxic to pursue. This evidence concerns the gene RPS6KB1 and breast carcinoma.