However, only 20% of cases of Brugada syndrome are associated with mutations in SCN5A, as in the majority of patients with Brugada syndrome genetic testing is unable to identify the genetic mutation responsible.[5] Over 290 mutations in the SCN5A gene have been discovered to date, each altering sodium channel function in subtly different ways.[2] This variation partially explains the differences in severity of the condition between different persons, ranging from a highly dangerous condition causing death at a young age to a benign condition that may not cause any problems at all. However, the genetics of Brugada syndrome are complex, and it is likely that the condition results from the interactions of many genes. Because of these complex interactions, some members of a family who carry a particular mutation may show evidence of Brugada syndrome while other carrying the same mutation may not, referred to as variable penetrance.[3]