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Id3, also known as inhibitor of DNA-binding/differentiation-3, is a transcription regulator. It is involved in multiple biological processes such as T-cell development and differentiation, macrophage polarization, and plays a role in various diseases including cancer. In T-cell development, it transiently acts downstream of extracellular signals like TCR signaling, influencing E-protein binding to target genes, which is crucial for T-cell commitment and differentiation [2]. In macrophages, it helps control the balance between activating and inhibitory receptors, thereby affecting their anti-tumor activity [1].

In loss-and gain-of-function experiments, ID3 was shown to be sufficient to endow macrophages with potent anti-tumor activity. ID3 deficiency promoted the metastatic ability of lung cancer cells through its effects on the transcriptional regulation of CDH1, indicating its tumor-suppressive role as a downstream effector of p53 [3]. In the context of T-cell function, ID3 deficiency significantly interrupted the maintenance of tumor-specific memory CD8+ T cells in draining lymph nodes during tumorigenesis, resulting in decreased tumor-infiltrating CD8+ T cells and impaired tumor control [4].

In conclusion, Id3 is a key transcription regulator involved in immune cell function and cancer-related processes. Model-based research, especially through gene knockout experiments, has revealed its importance in maintaining the balance of immune responses and suppressing tumor development, providing insights into potential therapeutic strategies for cancer treatment.