Nitrogen availability in soil is a key factor limiting plant yield. Plant success relies on rapid sensing of intrinsic N status and activation of molecular responses to adjust N use. Plants take up N mainly as NO3- and NH4+. NO3- is often the preferred N source, while excessive NH4+ uptake may be toxic. NO3- signalling affects many cellular processes, in tight link with auxin and CK signalling: through complex crosstalk, they orchestrate a communication network driving plant growth. My focus is on Cytokinin Response Factors (CRFs), a sub-branch of the AP2/ERF transcription factor superfamily. CRFs intersect auxin and CK signalling with stress responses. Recent reports link CRFs to NO3--induced transcriptional reprogramming1,2, modulation of root systems architecture in response to N availability2, and a role in integrating N sensing in roots via CK to auxin-guided shoot growth3. Yet, how CRFs are regulated during N sensing remains unclear. In silico and experimental evidence point toward post-translational control, which is dependent on the N source provided. Combining cell biology, genetics, proteomics, and physiology of Arabidopsis, I dissect the molecular layers of CRF regulation during N sensing and their role in modulating plant adaptive growth. Understanding reversible CRF regulation sheds new light on how plants adapt to changes in N availability, thus providing additional tools to optimise N utilization in increasingly harsher environments.