In particular, they found that perturbation of PPP significantly increased Nrf2 DNA binding to NR1D1 in U2OS cells, thus indicating that the Nrf2 activation may relay redox signals to circadian clock through NR1D1. Such results corroborate the hypothesis that Nrf2 represents a key nodal player between redox and circadian oscillations and provide a molecular mechanism explaining how redox imbalance, which is a key feature in many pathology (e.g. cancer, neurodegenerative and cardiovascular diseases), may disrupt circadian rhythmicity. Here, NR1D1 is linked to cardiovascular disorder.