expression in the culture was increased upon further differentiation into neurons (Fig. 5A, B). While the direction of the PAX6 effect in neurons is different, both of these BD iPSC studies are consistent with there being an alteration in the normal fate of neuronal differentiation in BD iPSCs. These differences may arise from the use of a different neuron/NPC differentiation protocol as in Chen et al., control and BD neurons were derived from iPSC aggregates in which neural induction was performed using dual SMAD inhibition with subsequent manual passaging and expansion of rosettes followed by differentiation into neurons; our NPC derivations begin in a monolayer and did not use dual SMAD inhibition. Alternatively, these differences may be inherent to the particular BD patients investigated. Similar to our results, Chen et al. also identified changes in the calcium channel subunit CACNA1E, although once again the direction of the change was different. Our data also suggest other calcium channel subunits are altered (e.g. CACNA1E, CACNA1G, CACNB1, CACNG8 (Fig. 5B)), consistent with calcium signaling being altered in neurons from BD patients. Another similarity in the gene expression data were FGF14 levels: both studies show FGF14 levels are increased in BD neurons. FGF14 is
