The past decades have seen a steady increase of interest in developing Igs as biotherapeutic agents for the treatment of various diseases, including cancer and autoimmune disorders.1, 2, 3 While the architectures of Igs are relatively conserved, they exhibit dramatic differences in their dynamics and mode of interactions with antigens and cognate receptors.4, 5 These differences stem from intrinsic features in their structures such as binding‐site specificity and hinge flexibility (Figure 1 a).6 This evidence concerns the gene CUBN and cancer.