People prone to mood disorders and anxiety typically show increased sensitivity to task‑irrelevant stimulation signifying threat. Better knowledge about the brain mechanisms mediating this sensitivity as well as about individual inherited differences in how these mechanisms function is a precondition for developing improved vulnerability screening, resilience building and treatment methods. The chances to have affective disorders are known to depend, among other factors, on the functioning of the brain serotonin systems developed under influence from common genetic variability. However, the extent and directions of the effects of SNPs involved in serotonergic regulation on the propensity for suboptimal threat‑sensitivity are poorly understood. This applies also to HTR1A rs6295 polymorphism. Assisted by our custom developed emotional attentional blink task, we found that nonclinical subjects carrying the G allele (compared to C allele homozygotes) had higher sensitivity to threat‑depicting distractor stimuli, expressed as an increase in the blink magnitude. We also disrupted right‑hemisphere dorsolateral prefrontal cortex by rTMS (repetitive transcranial magnetic stimulation) to look for the possible role of DLPFC (dorsolateral prefrontal cortex; known to be involved in cognitive control of responses to affective stimuli) in serotonergic regulation mediated by the HTR1A rs6295 polymorphism. No main effects or interactions with rTMS being involved were found.