Some amino acids with high selective betweenness centrality in the PSN may largely perturb the intramolecular communication pathways necessary for switching between GCAP1 regulatory modes, and the fact that some hubs are target of retinal dystrophy mutants suggests that the lack of complete inhibition of the target GC observed in many cases is likely due to the perturbation of these intermolecular routes. The gene discussed is GUCA1A; the disease is inherited retinal dystrophy.