Csf3r, also known as the receptor for colony-stimulating factor 3, plays a crucial role in the regulation of granulocyte production. It is a key component in the granulocyte colony-stimulating factor (G-CSF) signalling pathway, which is essential for the maturation, proliferation, and survival of neutrophil granulocytes [3].

Activating mutations in Csf3r are frequently found in chronic neutrophilic leukemia (CNL) and a subset of atypical chronic myeloid leukemia (aCML). In 59% of patients with CNL or aCML, such mutations were identified, and they lead to preferential downstream kinase signalling through SRC family-TNK2 or JAK kinases and differential sensitivity to kinase inhibitors [1]. Moreover, Csf3r mutations are not restricted to CNL. They can also occur in other myeloid neoplasms like acute myeloid leukemia (AML), chronic myelomonocytic leukemia, and myeloproliferative neoplasm, with different co-occurring mutations depending on the type of neoplasm [2].

In conclusion, Csf3r is essential for granulocyte-related biological processes. Research on Csf3r, especially its mutations, has significantly contributed to understanding the pathogenesis of myeloid neoplasms such as CNL and aCML. These findings may potentially lead to more accurate diagnoses and the development of targeted therapies for these diseases.