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Integrins act as mechanoreceptors, linking BCR activation to cytoskeletal remodeling, facilitating immune synapse formation, antigen recognition, and extraction. BCR activation models describe receptor clustering and mechanical changes within the antigen\u2013BCR complex. Upon activation, immune synapses form, enabling antigen extraction and downstream signaling. Integrins stabilize these synapses, amplify BCR signaling, and modulate BCR positioning\n                    <jats:italic>via<\/jats:italic>\n                    actin reorganization. In chronic lymphocytic leukemia (CLL), aberrant BCR signaling and integrins are major players in leukemic cell homing, prognosis, and therapy resistance. In this review, we summarize the current understanding of the interplay of BCR mechanics and B cell localization, with a particular focus on communication between BCR signaling and integrin\u2010mediated processes\n                    <jats:italic>via<\/jats:italic>\n                    actin dynamics. 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