It has been brought to our attention that there is an error in the poster published in association with this article. Non-phosphorylated ICAP1 is shown to bind to the cytoplasmic tails of integrin β-subunits, whereas Ca2+/calmodulin-dependent protein kinase II (CaMKII)-mediated phosphorylation of ICAP1 is depicted as driving dissociation of ICAP1 from integrin β-tails. Although ICAP1 is indeed a substrate for CaMKII, the phosphorylation of ICAP1 on Thr38 is likely to enhance ICAP1 binding to β1 tails rather than inhibit the interaction, and this might account for CaMKII-mediated inhibition of α5β1 activation (Bouvard et al., 1998; Bouvard and Block, 1998).