While basal DDIT4 gene expression might be beneficial in some (low-grade) tumours, it is the degree of potential adaptive upregulation of DDIT4, that is, the efficacy of an intact DDIT4 sensor to inhibit mTORC1 signalling in response to cellular stressors, that mediates therapy resistance (Fig. 5) as exemplified by the increased sensitivity of DDIT4sh cells to radiotherapy and chemotherapy (Fig. 3a, b). This evidence concerns the gene DDIT4 and neoplasm.