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max in WT synaptoneurosomes, suggesting that Src signaling could be downregulated in KI synapses. Then again, our capacity to rescue SERT purpose in KI midbrain synaptoneurosomes because of the inhibition of FAK suggests elevated FAK signaling downstream on the Pro32Pro33 mutant, as confirmed by enhanced pFAK localization in 5-HT synapses. Our information as a result recommend the Src–FAK pathway is uncoupled by constitutive activation of integrin β3, and thus Every kinase could be influencing SERT independently.