Neisseria meningitidis is a major cause of meningitis and sepsis worldwide. Why some individuals are more susceptible than others to meningococcal disease is not fully understood but individuals with defects in the terminal complement pathway are at higher risk of developing meningococcal disease. Genome wide association studies have identified polymorphisms in factor H and factor H related protein-3, which are linked with susceptibility to meningococcal disease. Here we propose a mechanism whereby competition between these two proteins for a single molecule on the bacterial surface, governed by the relative serum levels of both proteins can influence host susceptibility to meningococcal disease.