This is completely novel evidence; the notion of a splicing adaptation to PINK1-deficiency is currently supported only by an OMICS study into posttranslational modifications of the brain in a genetic mouse model of PD, where a strongly altered arginine-methylation of the splicing factor PSF was observed, caused either by PINK1 deficiency or by alpha-synuclein gain of function [22]. The gene discussed is PINK1; the disease is Parkinson disease.