Kitl, also known as stem cell factor (SCF), is a paracrine signaling factor playing crucial roles in multiple biological processes. It is involved in maintaining tissue homeostasis, regulating hematopoietic stem cell function, and is essential for melanocyte development [1,2,3,5]. It participates in signaling pathways that impact cell proliferation, differentiation, and self-renewal [1,5]. Genetic models, such as gene-knockout (KO) and conditional-knockout (CKO) mouse models, are valuable tools for studying Kitl's functions.

In hematopoietic aging, reduced Kitl expression in mesenchymal stromal cells (MSCs) of middle-aged mice was highly correlated with reduced lymphoid lineage commitment of hematopoietic stem cells (HSCs) and increased signatures of differentiation-inactive HSCs [1]. In pancreas tissue, genetic inhibition of mesenchymal Kitl increased tumor growth and reduced survival of tumor-bearing mice, indicating that loss of stromal Kitl creates a tumor-permissive microenvironment [2,4]. In postnatal and adult mice, overexpression of Kitl in melanocytes influenced their proliferation, differentiation, and the self-renewal capacity of melanocyte stem cells, and also induced melanocyte migration from hair follicles to the epidermis [5]. Conditional deletion of Scf (Kitl) from endothelial cells or leptin receptor (Lepr)-expressing perivascular stromal cells depleted HSCs from the bone marrow [6].

In conclusion, Kitl is essential for maintaining tissue homeostasis, regulating hematopoietic stem cells, and influencing melanocyte development. Studies using KO/CKO mouse models have revealed its significant role in hematopoietic aging, pancreas tumor progression, and melanocyte-related processes. Understanding Kitl's functions provides insights into these biological processes and potential therapeutic targets for related diseases.