It is known that suicidal behaviour has multiple causes. If triggers could be mainly attributed to environmental factors, predisposition could be associated with early stressors on one side such as childhood adversities and genetic predisposition. No convincing animal model of suicide has been produced to date. The study of endophenotypes has been proposed as a good strategy to overcome the methodological difficulties. However, research in suicidal behaviours using endophenotypes entrails important methodological problems. Further, serotoninergic system was studied in patients with suicidal behaviour primary due to its involvement of serotonin in impulsive-aggressive behaviour, which has been shown to be a major risk factor in suicidal behaviour. Not only on the level of neurotransmitters but also the regulation of neurotropic factors could be impaired in suicide victims. Multiple lines of evidence including studies of levels of BDNF in blood cells and plasma of suicidal patients, postmortem brain studies in suicidal subjects with or without depression, and genetic association studies linking BDNF to suicide suggest that suicidal behaviour may be associated with a decrease in BDNF functioning. It seems that especially specific gene variants regulating the serotoninergic system and other neuronal systems involved in stress response are associated with suicidal behaviour. Most genetic studies on suicidal behaviour have considered a small set of functional polymorphisms relevant mostly to monoaminergic neurotransmission. However, genes and epigenetic mechanisms involved in regulation of other factors such as BDNF seem to be even more relevant for further research.