This observation supports the idea that FOS might contribute to the rescue of neuronal differentiation by activating (at least to some extent) genes that are downregulated in the absence of Sox2. Indeed, it is interesting that several genes that are known to be essential for correct differentiation of various neuronal types are among the common FOS/SOX2 targets (Figure 4 and Figure 5 and related references in text); some of these, when mutated, cause brain disease in humans. Here, FOS is linked to brain disorder.