Furthermore, overexpression of wild-type PINK1 increases mitochondrial interconnectivity and suppresses toxin-induced autophagy, whereas knockdown of PINK1 expression potentiates mitochondrial fragmentation and induces autophagy [197], suggesting that induced autophagy as a consequence of loss of function of PINK1 may contribute to the pathogenesis of PD. Here, PINK1 is linked to Parkinson disease.