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Twelve\u2010month remission from seizures is less likely in female patients, individuals aged 11\u201336\u00a0years and those with neurological insults and shorter time between first seizure and starting treatment. It has been found that the presence of multiple seizures prior to diagnosis is a risk factor for pharmacoresistance and is correlated with epilepsy type as well as intrinsic severity. The key role of neuroinflammation in the pathophysiology of resistant epilepsy is becoming clear. Our work in this area suggests that high\u2010mobility group box 1 isoforms may be candidate biomarkers for treatment stratification and novel drug targets in epilepsy. Furthermore, transporter polymorphisms contributing to the intrinsic severity of epilepsy are providing robust neurobiological evidence on an emerging theory of drug resistance, which may also provide new insights into disease stratification. Some of the rare genetic epilepsies enable treatment stratification through testing for the causal mutation, for example <jats:italic><jats:styled-content style=\"fixed-case\">SCN<\/jats:styled-content>1<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content><\/jats:italic> mutations in patients with <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>ravet's syndrome. Up to 50% of patients develop adverse reactions to <jats:styled-content style=\"fixed-case\">AED<\/jats:styled-content>s which in turn affects tolerability and compliance. Immune\u2010mediated hypersensitivity reactions to <jats:styled-content style=\"fixed-case\">AED<\/jats:styled-content> therapy, such as toxic epidermal necrolysis, are the most serious adverse reactions and have been associated with polymorphisms in the human leucocyte antigen (<jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>) complex. Pharmacogenetic screening for <jats:italic><jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>*15:02<\/jats:italic> in <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>sian populations can prevent carbamazepine\u2010induced <jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>tevens\u2013<jats:styled-content style=\"fixed-case\">J<\/jats:styled-content>ohnson syndrome. We have identified <jats:italic><jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>*31:01<\/jats:italic> as a potential risk marker for all phenotypes of carbamazepine\u2010induced hypersensitivity with applicability in <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>uropean and other populations. 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