In contrast, there was apparent upregulation of these analytes in the specimen from the IGF1R-resistant tumor that emerged during IGF1R antibody therapy, with predominant nuclear expression of both p-mTOR (Ser2448) and p-Akt (Ser473), consistent with mTORC2 pathway activation [17], [20], [21]. The gene discussed is IGF1R; the disease is neoplasm.