In a working hypothesis in keeping with our previous SCD inhibitor findings, we suggest two mechanisms for increased αS membrane binding in PD-mutant neurons: (1) enhanced membrane fluidity due to the increased incorporation of unsaturated fatty acyl side chains; and (2) possible binding of αS directly to monounsaturated FAs incorporated as fatty acyl side chains into a phospholipid membrane19,20. This evidence concerns the gene SCD and Parkinson disease.