Sltm, also known as SAFB-like transcription modulator, is a chromatin-associated protein with DNA and RNA binding capacities. It belongs to the SAFB family and is involved in multiple biological processes. It has been implicated in pathways such as the Notch pathway, and is important for the transcriptional regulation in the Sonic hedgehog (SHH) signaling pathway [2,3].

In a gene-based rare variant association study, rare heterozygous loss-of-function of Sltm was found to increase adult body mass index (BMI) in men, suggesting its role in the genetic regulation of obesity [1]. In hepatocellular carcinoma, hypoxia-induced DTL promotes the ubiquitination and degradation of Sltm, which in turn activates the Notch pathway, promoting cancer cell proliferation, metastasis, and sorafenib resistance [2]. In an in vivo study, Sltm deletion through Nuclease technology-mediated gene editing in mice caused perinatal lethality and SHH-related abnormal ventral neural tube phenotypes, indicating its crucial role in embryonic development [3].

In conclusion, Sltm plays essential roles in processes like obesity-related genetic regulation, cancer development, and embryonic development. The use of gene knockout models, such as the Nuclease technology-mediated Sltm deletion in mice, has been instrumental in revealing these functions, providing insights into potential disease mechanisms and therapeutic targets in areas like obesity and hepatocellular carcinoma [1,2,3].