We report that park or Pink1 KD in young flies modulated proteostatic modules in a tissue-dependent manner; ubiquitously increased cell oxidative load (shown also after loss-off PINK1 function in SH-SY5Y human neuroblastoma cells [35]), and suppressed mitophagy in neuronal and muscle tissues causing mitochondrial aggregation and neuromuscular degeneration. The gene discussed is PINK1; the disease is neuroblastoma.