The other major group of HypoKPP is due to missense mutations in the voltage sensor of domain 2 of SCN4A (the same sodium channel affected in HyperKPP and paramyotonia congenita).[4] There is some genotype/phenotype correlation—for example, acetazolamide treatment is often deleterious in the R672G mutation of the SCN4A gene. The gene discussed is SCN4A; the disease is hyperkalemic periodic paralysis.