Alpha-Smooth muscle actin (α-SMA) is used as a marker for a subset 3 of activated fibrogenic cells, myofibroblasts, which are regarded as 4 important effector cells of tissue fibrogenesis. We addressed whether ASMA 5 gene (actin alpha 2 gene or ACTA2) expression is upregulated in in cases 6 with BM fibrosis compared to those with no BM fibrosis in order to evaluate 7 its role in the pathogenesis of BM fibrosis. ASMA expression was detected 8 by quantitative RT-PCR in formalin fixed paraffin embedded (FFPE) bone 9 marrow trephine biopsy samples of cases with neoplastic bone marrow 10 diseases as well as reactive bone marrow disorders cases. Both groups 11 included cases with and without bone marrow fibrosis. Results indicated that 12 there was no statistically significant difference in ASMA (ACTA2) gene 13 expression between neoplastic fibrotic and non-fibrotic cases as well as 14 between reactive fibrotic and non-fibrotic cases. Also the level of α-SMA 15 expression does not correlate positively with the grade of bone marrow 16 fibrosis. We conclude that α-SMA alone can‟t be considered a functional 17 marker of fibrogenic cells in bone marrow fibrosis. Exploration of other 18 related genetic pathway is recommended.