Therefore, it is tempting to speculate that, in response to metabolic conditions that modify the redox state (e.g., hyperglycemia), NRF2 activation may calibrate the HIPK2 activation through, for instance, post-translational modifications [91] which impair HIPK2 apoptotic activity, favoring instead the transcription of genes promoting chemoresistance and tumor progression. The gene discussed is HIPK2; the disease is Hyperglycemia.