These results demonstrate that 1) p53 status (expression) can determine the effect of IGF-1R inhibition on cancer cell responses to CP, and 2) crosstalk between the IGF-1R/AKT/mTORC1 pathway and p53 and p27 can reduce cancer cell responsiveness to chemotherapy (CP), which could ultimately limit the effectiveness of IGF-1R pathway inhibitors in the clinic. The gene discussed is AKT1; the disease is cancer.