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, 2014), and indeed mutations on this gene have been linked to some forms of ASD (Maekawa et al., 2009). Importantly, PAX6 is coexpressed with AUTS2 in the ventricular and subventricular regions (Bedogni et al., 2010a). PAX6 has been shown to be involved in interhemispheric transfer (Bamiou et al., 2004), to the extent that mutations in this gene result in working memory problems (Bamiou et al., 2007). Moreover, PAX6 plays an important role in the development of thalamic connections. Specifically, mammillo-thalamic tracts were missing in Pax6 mutant mice (Valverde et al., 2000). Repression of Shh by Pax6 regulates diencephalic patterning by controlling the central diencephalic organizer (Caballero et al., 2014). Additionally, Pax6 regulates the orientation and mode of cell division of progenitors in the mouse cerebral cortex, influencing as it does cell adhesion during Ponatinib cortical development (Tyas et al., 2003). In this context, it interacts with many of the genes discussed in the previous subsection, and gives rise to cortical layering abnormalities when knocked-out in mice (e.g., Tuoc et al., 2009). Pax6 plays as well a crucial role at the level of the cortical hem, which regulates both the size and patterning of the cortex (Caronia-Brown et al., 2014), but also at the cortical anti-hem (Subramanian et al., 2009). Positioned as a mirror image of the cortical hem, along the lateral margin of the cortical primordium, the cortical anti-hem is identified by gene expression for three epidermal growth factor family members, Tgf��, Nrg1, and Nrg3, as well as two other signaling molecules, Fgf7 and the secreted Wnt antagonist Sfrp2. The anti-hem is lost in mice homozygous for the Pax6 mutation. It is worth mentioning in this context that both FGF7 and NRG3 are among the genes that show signals of a selective sweep in AMHs compared to Neanderthals (Green et al., 2010; Pr��fer et al., 2014). A heterozygous mutation of PAX6 has been shown in individuals with aniridia and deficits in executive and social cognition. Structural abnormalities of gray matter were reported in the anterior cingulate cortex, the cerebellum and the medial temporal lobe, as well as white matter deficits in corpus callosum. Functional MRI demonstrated reduced activation of fronto-striato-thalamic systems during performance of overt verbal fluency and non-sense sentence completion; the most consistent abnormality of verbal executive activation was located in the thalamus (Ellison-Wright et al., 2004). Eye problems associated with PAX6 deficiencies are also worth bearing in mind in light of the potential cognitive relevance of eye size in Neanderthals and AMHs (Pearce et al., 2013), as we reviewed in the first section of the paper.