While such a proposed mechanism is generic and simplistic, post-mortem assessment of brain tissues from a PD patient with the heterozygous CHCHD2 T61I mutation demonstrate the accumulation of soluble and insoluble S129 phospho-α-synuclein, as well as increased insoluble CHCHD2 and CHCHD10 (Ikeda et al., 2019). This evidence concerns the gene CHCHD10 and Parkinson disease.