Lrig1, or leucine-rich repeats and immunoglobulin-like domains protein 1, is an important regulator in multiple biological processes. It acts as an endogenous feedback regulator of receptor tyrosine kinases (RTKs), especially antagonizing the expression and activities of ERBB and other RTKs [2,4,5]. It is involved in regulating stem cell quiescence and has tumor-suppressive functions in several cancers [2].

In T-cell-specific Lrig1-deleted mice, superior antitumor responses were observed due to the expansion of tumor-specific cytotoxic T lymphocytes (CTLs) with enhanced effector function and survival, suggesting Lrig1 as an inhibitory immune checkpoint receptor [1]. In adult neural stem cells, genetic disruption of Lrig1 in vivo led to enhanced proliferation, indicating its role in regulating the exit from quiescence [3]. In the context of colon development, an inducible knockout of Lrig1 showed that it restrains proliferation within a critical developmental time window [6]. In adult neural stem cells, Lrig1 knockout models demonstrated that Lrig1 controls proliferation through facilitating TGFβ and BMP signalling pathways [7].

In conclusion, Lrig1 plays essential roles in regulating stem cell quiescence, restraining cell proliferation, and acting as a tumor suppressor in some cancers. Mouse knockout models have been crucial in revealing these functions, especially in the areas of cancer immunotherapy, neural stem cell regulation, and colon development [1,2,3,6,7].