Increasingly, recognition of genetic epilepsies has become more than just making a diagnosis. Understanding the molecular etiology may lead to improved understanding of prognosis, a change in treatment, anticipatory guidance for the patient and family members, and ultimately improved outcomes. Indeed, Dravet syndrome is a prime example of how molecular diagnosis benefits patient care. Identifying Dravet syndrome in the setting of SCN1a mutation informs avoidance of medications known to exacerbate the epilepsy (ie, antiseizure medications with sodium channel mechanisms) and selection of medications most effective for the condition. In addition, multiple drugs have recently been approved for Dravet syndrome and diagnosis opens the door to additional research trials specific to this population. Even more compelling are precision treatments on the horizon utilizing antisense oligonucleotides, viral vector therapies, and drugs targeting the Nav 1.1 channel, promising the potential to truly modify the course of the disease. One assumes earlier treatment will be associated with more favorable outcome, but there may still be benefits later in life. Dravet syndrome is not alone, as there are several conditions for which a molecular diagnosis may change therapeutic decision-making including GLUT-1 deficiency and sodium channelopathies such as SCN2a and SCN8a.