Meis1, or myeloid ecotropic viral integration site 1, belongs to the homeobox containing transcriptional regulatory network (HOX). It encodes a transcription factor essential during development and is involved in multiple intracellular signaling pathways [1,3,5]. Meis1 has been associated with various biological processes and diseases, such as hematopoiesis, embryonic patterning, eye development, and diseases like restless legs syndrome (RLS) and cancers [1,3,4,6].

In RLS, GWAS identified risk variants in non-coding regions of Meis1. Mouse studies showed that heterozygous Meis1 inactivation causes hyperactivity at the onset of the inactive period, mimicking human RLS, and reveals its effect on the dopaminergic system [1,7]. In colorectal cancer, downregulation of Meis1 mediated by ELFN1-AS1/EZH2/DNMT3a axis promotes tumorigenesis and oxaliplatin resistance, while Meis1 overexpression impairs cell viability and enhances oxaliplatin sensitivity [2]. In the context of cardiovascular regeneration, inhibition of Meis1 expression increases neonatal mouse cardiomyocyte proliferative capacity, while overexpression reduces the length of the proliferative window [3].

In summary, Meis1 plays crucial roles in development, cell proliferation, and differentiation, and is implicated in diseases like RLS and cancers. Mouse models, including gene knockout or conditional knockout models, have been instrumental in revealing these functions, providing insights into the underlying mechanisms and potential therapeutic targets for these disease areas.