The amino-acid tyrosine (TYR) is thought to modulate cognitive functions that are driven by dopamine (DA), as consumption of TYR enhances DA levels in the brain (Gibson and Wurtman, 1977; Cuche et al., 1985). It could therefore reverse decreases in DA level that are detrimental for cognitive performance (Muly et al., 1998; Goldman-Rakic et al., 2000; Nieoullon, 2002). So far, TYR has been considered not so much as an enhancer of healthy cognitive functioning but rather as a means to reduce the negative side-effects of dopamine-related pathologies, such as Parkinson's disease (Growdon et al., 1982; Lemoine et al., 1989), phenylketonuria (van Spronsen et al., 1996), depression (Gelenberg and Gibson, 1984), and attention deficit hyperactivity disorder (Wood et al., 1985). However, the outcomes were mixed: some patients reported significant improvements, while other did not. In clinical samples some variation in response may be explained by impaired processes such as DA synthesis, which would lessen or even completely prevent an effect of TYR. But even healthy samples differ in response to TYR supplementation, which suggests that clinically impaired DA function is not the only source of variation. The focus of the present opinion article is not on clinical populations but on TYR effects on cognitive control in healthy humans. In healthy individuals, TYR has often been used to reduce the negative effects of conditions that deplete the brain's dopaminergic resources, such as extreme stress. The supply of TYR was found to reduce stress-induced impairments of working memory and attentional tasks, but more so in individuals who were particularly sensitive to the stressors (Deijen and Orlebeke, 1994; Shurtleff et al., 1994; Mahoney et al., 2007). Even without exposure to stress, administration of TYR has been shown to have an acute beneficial effect on task-performance thought to be related to DA, e.g., simultaneously performing multiple tasks (Thomas et al., 1999), the updating and monitoring of working memory (Colzato et al., 2013a), and inhibitory control (Colzato et al., 2014a). Taken together, in healthy humans TYR seems to work against what has been coined “ego-depletion”—the exhaustion of limited cognitive control (CC) resources (Baumeister et al., 1998). Demanding tasks may deplete the available control resources more, especially in individuals having fewer resources and/or those that suffer more from the situational demands, and TYR may be able to replete the missing resources to some degree. This possibility should not be surprising given that CC relies on DA (Cools, 2006). The hypotheses that DA is one of the depleted resources and TYR reverses its depletion are consistent with the idea that there is an optimal level of DA at which cognitive performance peaks while it suffers at lower levels (Muly et al., 1998; Goldman-Rakic et al., 2000; Nieoullon, 2002). Given that TYR raises the DA level, we argue that TYR can enhance cognitive performance in healthy individuals whenever one has a lower than optimal DA level. Besides individual differences in the response to task-induced depletion, DA level also seems to vary between healthy individuals in a more stable and enduring fashion (Cools, 2006; Cools et al., 2008, 2009). This suggests that individuals differ in how far away they are from their optimum, i.e., some individuals have a lot of room for improvement, while others may already have an optimal, or even a higher-than-optimal DA level. We expect that individuals with an optimal baseline have little left of the enzyme called tyrosine-hydroxylase, which converts TYR into DA (Daubner et al., 2011). This means that they have little risk of overdosing from TYR supplementation, instead they should experience hardly any change in performance. Given that individuals can vary in their response to TYR supplementation, it is necessary that future studies on TYR take into account individual differences, so to ensure that samples are comparable and results are generalizable. To this end we discuss a number of DA-related measures and factors that could predict or modulate the effect of TYR supplementation. This is by no means an exhaustive list; the aim of this opinion article is rather to point out and highlight some accessible predictors of DA function that may help to improve designing future TYR studies and making the analyses of their outcomes more informative. To this date, the individual differences discussed below have not yet been investigated in combination with TYR. However, based on literature that details their relation to DA function we argue that these individual differences will prove fruitful for future research.