The dopaminergic neuron population within midbrain organoids produces dopamine and has pacemaker activity.15 These features can justify the higher vulnerability of the dopaminergic neuron population to stress and energy loss driven by the p.R272Q Miro1 mutation within organoids, modelling the main hallmark of PD.2 Likewise, the loss of TH+ neurons in the midbrain organoid model has also been described in familial forms of PD, including LRRK2, PINK1 and GBA mutations.19, 20, 27. The gene discussed is LRRK2; the disease is Parkinson disease.