Rarb, or retinoic acid receptor beta, is a transcriptional regulator crucial for coordinating retinoic acid (RA)-mediated morphogenic movements, cell growth, and differentiation [4]. It is involved in the retinoic acid signaling pathway, which has significant importance in multiple biological processes including eye development, hematopoiesis, and neural development [4,5,6]. Genetic models such as knockout (KO) or conditional knockout (CKO) mouse models can be valuable for studying its functions.

In gastric cancer, knockdown of Rarb in vitro accelerated cancer cell proliferation, invasion, and migration, and promoted epithelial-mesenchymal transition (EMT) [1]. In acute promyelocytic leukemia (APL), the majority of RARA-negative APL cases had RARB translocations, and the TBL1XR1-RARB fusion protein exerted similar oncogenic effects to PML-RARA, although the response to retinoids was attenuated [2]. In colorectal carcinoma, overexpression of Rarb inhibited the properties of cancer stem cells (CSCs) and enhanced radiotherapy sensitivity, and DNA methylation inhibitor treatment improved radiotherapy sensitivity by promoting Rarb expression [3].

In conclusion, Rarb plays essential roles in multiple biological processes including cell growth, differentiation, and development. Through model-based research, it has been shown to be involved in various disease conditions such as gastric cancer, APL, and colorectal carcinoma. Understanding Rarb's functions can provide insights into disease mechanisms and potential therapeutic targets.