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Cytoskeletal remodeling contributes to these mechanisms, where the hematopoietic protein HS1 appears to play a key role. Thus, we generated C57BL\/6 HS1 knockout (HS1KO) mice to assess its impact on lymphocyte development. Young HS1KO mice showed some alterations in B cell maturation and T cell differentiation, which appeared to normalize with age. In double-transgenic E\u03bc-TCL1-HS1KO mice, combining HS1 loss with the standard E\u03bc-TCL1 CLL mouse model, we observed a trend of reduction in the CD4\/CD8 ratio, and disrupted splenic architecture with loss of follicular organization. Transcriptomic and kinase profiling of the human CLL cell line MEC1, in which HS1 was knocked out (MEC1-HS1KO), revealed a coherent impairment in terms of cell mobility as highlighted by severely impaired migration in 2D and 3D environments, reduced chemotactic responses to CXCL12 and CCL19; deregulation of cytoskeletal, adhesion, and apoptotic pathways; and increased resistance to apoptosis. We posited that these defects could reduce sensitivity to BTK (Bruton's tyrosine kinase) inhibition, a standard therapeutic approach in CLL. Primary CLL cells from the spleen of E\u03bc-TCL1-HS1KO mice appeared to show reduced sensitivity to ibrutinib, a finding that was also observed in adoptive transfer experiments designed to equalize disease burden. Wild-type mice receiving E\u03bc-TCL1-HS1KO leukemic cells tend to be more resistant to ibrutinib, particularly in the peripheral blood and spleen. All together, these findings establish HS1 as a potential regulator linking B cell receptor signaling, cytoskeletal remodeling, leukemic progression, and response to therapy, supporting its potential as a biomarker for BTK inhibitor sensitivity.<\/jats:p>","DOI":"10.1093\/jleuko\/qiag099","type":"journal-article","created":{"date-parts":[[2026,7,13]],"date-time":"2026-07-13T11:28:02Z","timestamp":1783942082000},"source":"Crossref","is-referenced-by-count":0,"title":["HS1 loss drives cytoskeletal dysregulation and reduces sensitivity to BTK inhibition in chronic lymphocytic leukemia"],"prefix":"10.1093","volume":"118","author":[{"given":"Luca","family":"Russo","sequence":"first","affiliation":[{"name":"Malignant B Cells Biology and 3D Modelling Unit, Division of Experimental Oncology, Comprehensive Cancer Centre, IRCCS Ospedale San Raffaele , Via Olgettina 58, Milan 20132 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