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Human behavior is driven by automatic and deliberative processes. In contrast to fast automatic processing, deliberative processes rely on cognitive control. Substance use disorders (SUD) are featured by an imbalance of automatic and deliberative behavioral regulation. Errormonitoring is one aspect of cognitive control affected by SUD. Error-monitoring is the prerequisite for the adaption of automatized behaviors with unfavorable outcomes. Impairments in cognitive control in SUD are accompanied by cue-reactivity, the automatized response to drug-related cues. Both mechanisms are related to the severe impairments in decision making in SUD. Cue-reactivity is established via repeated consumption of a drug and is expressed at an autonomic (sympathetic activity), cognitive (craving) and behavioral (drug-seeking behavior) level. The 1-year abstinence rate for SUD treatment is 40-60%, which depicts the challenging modification of cue-reactivity involved in relapse (McLellan et al., 2000). The aim of this work was the transfer of the concept of mindfulness on the relation of cuereactivity and cognitive control. Accordingly, neuroscientific approaches focusing on this context will be discussed. The transfer of experimental research in this field to clinical practice allows developments in SUD treatment. Complementary, observations from clinical practice contribute to a better understanding of natural human brain functioning. This allows the establishment of eligible neuroscientific paradigms in reverse. Both views will be addressed within this work. The discussion is based upon results of four studies: Study 1: Visual alcohol cue-reactivity was analyzed in heavy social drinkers (HD) and light social drinkers (LD). Cue-reactivity was found in HD at an early attentional processing level (P100 latency) and during the processing of motivational significance (LPP amplitude). P100 latency and LPP amplitude predicted Alcohol Use Disorder Identification Test (AUDIT) scores. These effects were specifically found in relation to the recognition of alcohol content, not in the visual-feature control condition with unrecognized scrambled beverage pictures. Effects were driven by alcoholic-content, not the visual features of the pictures. Therefore, results encouraged the use of individualized stimulus-sets in cue-reactivity paradigms. 10 Study 2: Cue-reactivity effects on error-monitoring were measured in HD and LD, using simultaneous functional near-infrared spectroscopy (fNIRS) and electroencephalography (EEG). Although errormonitoring (error-related negativity, ERN/ error negativity, Ne) was affected by visual alcoholic cues in HD, there was no impairment at the behavioral level. Conclusively, differences in errorcompensation strategies between HD and LD were discussed. Study 3: Cue-reactivity and cognitive control were assessed during in-vivo smoking cue-exposure in smokers and non-smoking controls. Besides fNIRS measurement of the prefrontal cortex, subjects rated their craving verbally during cue-exposure. Craving was selectively elicited in smokers. Hemodynamic activity in the dorsolateral prefrontal cortex (dlPFC) and the orbitofrontal cortex (OFC) did not differ significantly between groups. Nevertheless, functional connectivity between dlPFC and OFC was significantly increased in smokers. Study 4: Immediate effects of transcranial direct current stimulation (tDCS) on cue-reactivity and cognitive control during smoking cue-exposure were measured via fNIRS, craving and heart-rate variability (HRV). HRV was added as measure to assess the autonomic level of cue-reactivity. Anodal tDCS over the left dlPFC with the cathode above OFC significantly increased functional connectivity during smoking cue-exposure in smokers. This effect neither affected HRV nor craving ratings.