A proposed mechanism of ultrasensitivity, called allovalency, suggests that activity "derives from a high local concentration of interaction sites moving independently of each other" 
Allovalency was first proposed when it was believed to occur in the pathway in which Sic1, is degraded in order for Cdk1-Clb (B-type cyclins) to allow entry into mitosis. Sic1 must be phosphorylated multiple times in order to be recognized and degraded by Cdc4 of the SCF Complex. Since Cdc4 only has one recognition site for these phosphorylated residues it was suggested that as the amount of phosphorylation increases, it exponentially increases the likelihood that Sic1 is recognized and degraded by Cdc4. This type of interaction was thought to be relatively immune to loss of any one site and easily tuned to any given threshold by adjusting the properties of individual sites.  Assumptions for the allovalency mechanism were based on a general mathematical model that describes the interaction between a polyvalent disordered ligand and a single receptor site 
It was later found that the ultrasensitivity in Cdk1 levels by degradation of Sic1 is in fact due to a positive feedback loop.