Cebpz, also known as CAATT-box binding protein, is involved in multiple biological processes. It has been associated with pathways related to ribosomal RNA (rRNA) processing, and is thought to play a role in maintaining the balance of cell differentiation and proliferation. Genetic models are valuable for studying its functions in different physiological and pathological conditions [3].

In glucocorticoid-associated osteonecrosis of the femoral head, exosomal miR-1a-3p from glucocorticoid-stimulated M1 macrophages promotes the adipogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) by targeting Cebpz. Inhibiting miR-1a-3p expression mitigates the preferential adipogenic differentiation of BMSCs, suggesting Cebpz has a role in the pathogenesis of this disease [1]. In autophagy-dependent melanoma, Cebpz, as a component of the PERK-dependent endoplasmic reticulum (ER)-stress response, upregulates interleukin-24 (IL24) expression upon PIKFYVE inhibitor treatment, leading to cell death [2].

In conclusion, Cebpz is essential in processes like adipogenic differentiation and ER-stress response-mediated cell death. Studies using relevant models have revealed its significance in diseases such as glucocorticoid-associated osteonecrosis of the femoral head and autophagy-dependent melanoma, providing potential therapeutic targets for these conditions.