Experimental evidence has demonstrated that, in PD conditions, over-activation of c-Abl might induce parkin dysfunction (Imam et al., 2011; Gonfloni et al., 2012; Dawson and Dawson, 2014), a-synuclein aggregation (Hebron et al., 2013a; Mahul-Mellier et al., 2014; Brahmachari et al., 2016), and impaired autophagy of toxic elements (Ertmer et al., 2007; Yogalingam and Pendergast, 2008; Xu et al., 2017), leading to the death of the nigral dopaminergic cells. Here, ABL1 is linked to Parkinson disease.