Because treatment with the in vivo-validated SCD inhibitor 5b34 prevented the decreased T:M ratio of αSyn in both the G2019S and R1441C human neurons (as it does for fPD-mutant αSyn), we speculate that the mutant LRRK2-driven dyshomeostasis of αSyn may arise from altered fatty acyl composition of certain membranes that is important for proper transient αSyn-membrane binding and tetramer formation (discussed in ref. 32), as may also occur in the synucleinopathy caused by GBA1 loss-of-function mutations29. Here, SCD is linked to synucleinopathy.