Perturbations in the Rsp5/Bul1 protein degradation pathway have also been implicated in the tolerance to α‐synuclein, the protein that forms Lewy bodies in Parkinson's and other neurodegenerative diseases (Tardiff et al., 2013), suggesting perhaps that the Bul1 mutation could promote protein homeostasis via amelioration of the protein aggregate formation common to disome strains (Oromendia et al., 2012). This evidence concerns the gene NEDD4L and Parkinsonism.