Background and Aims: Cirrhosis patients exhibit cyto-penia, and, at times refractory neutropenia to granulocyte colony-stimulating factor (G-CSF), which acts through the CSF3-receptor (CSF3R), and changes in CSF3R can affect the response. We conducted this study to assess the CSF3R status and its relevance in cirrhotic patients. Methods: Cirrhotic patients (n=127) and controls (n=26) with clini-cally indicated bone marrow (BM) examination were stud-ied. BM assessment was done by qRT-PCR and immunohis-tochemistry (IHC) for CSF3R. Circulating G-CSF, CSF3R, and carcinoembryonic antigen cell adhesion molecule-1 (CEACAM1) were measured. BM hematopoietic precursor cells and their alterations were examined by flow cytom-etry. The findings were validated in liver cirrhosis patients who received G-CSF for severe neutropenia. Results: The mean age was 48.6±13.4 years, and 80.3％ were men. Circulatory CSF3R reduction was noted with the advance-ment of cirrhosis, and confirmed by qRT-PCR and IHC in BM. CSF3R decline was related to decreased hematopoietic stem cells (HSCs) and downregulation of CSF3R in the re-maining HSCs. Cocultures confirmed that CEACAM1 led to CSF3R downregulation in BM cells by possible lysosomal degradation. Baseline low peripheral blood-(PB)-CSF3R also predisposed development of infections on follow-up. Decreased CSF3R was also associated with nonresponse to exogenous G-CSF treatment of neutropenia. Conclu-sions: Advanced liver cirrhosis was associated with low CSF3R and high CEACAM1 levels in the BM and circula-tion, making patients prone to infection and inadequate response to exogenous G-CSF.