Conventional Vps35 deletion in mice (Vps35-/-) results in early embryonic lethality, but the heterozygous animals (Vps35+/-) are viable (Wen et al., 2011) and display PD relevant neuropathology, including accumulation of α-synuclein, loss of DA neurons, reduction of dopamine, and impairment of locomotor activity (Tang et al., 2015a). The gene discussed is VPS35; the disease is Parkinson disease.