Dr. Sergiu Pașcă

And that's very important because it couples electrical activity of the network with chemical activity inside the cells.

And what we knew about that mutation at that point, and that's pretty much all we knew in those early days, is that it probably...

allows the channel to stay open slightly longer, just a little bit longer.

So more calcium would go inside the cells.

Of course, there would be no way to know because you can't get a neuron or a cardiac cell from those patients to actually test it.

So what we did is essentially we made, we recruited some of these patients, we flew them to Stanford.

Then we got a tiny skin biopsy, made this iPS cells.

This takes months.

This takes already like four or five months.

And then we took those cells in a dish, started to deriving neurons.

And after about five, six, seven weeks, then we put them under a microscope and we started looking at the calcium.

You can measure calcium inside cells through a microscope and just literally look at it.

And I'll never forget that day, you know, when we did that experiment, was looking down the microscope and we essentially stimulated the neurons and you could just see how control cells will go.

Calcium goes inside the cells and then it goes out.

And then in patients that had Timothy syndrome, so in Timothy syndrome-derived neurons, you could see how the calcium will go, and then it will stay longer.

It takes longer to go out.

So it's like the first defect that we saw in patient-derived neurons that were actually not coming from a biopsy.

They were not coming.

So that was incredibly exciting, as you can imagine.

But it was still relatively simplistic, just a few neurons at the bottom of a dish.