Therefore, the aims of this study were: i) to investigate the involvement of integrins, specifically RGD – recognising integrins, in the mechano-response of human AF cells following treatment with 1.0 Hz CTS; ii) to investigate the activation of FAK via tyrosine 397 phosphorylation in human AF cells exposed to 1.0 Hz CTS and to determine whether FAK activation was integrin-dependent; and iii) to ascertain whether the previously reported altered mechanotransduction pathway operating in AF cells derived from degenerate tissue [22] was due to altered integrin involvement. Here, PTK2 is linked to atrial fibrillation.