Although the reason for this difference is currently unclear, one possibility is that tumour-specific microenvironments other than simple hypoxia, such as a decrease in the availability of glucose as well as oxygen, may be important for the activity of the UCHL1–HIF-1 axis based on the results of our in vitro experiment; the impact of UCHL1 on HIF-1α stability was facilitated when glucose concentrations decreased under hypoxic conditions (Supplementary Fig. 19). Here, UCHL1 is linked to neoplasm.