In contrast, with expression of large amounts of N-terminal mutant HTT fragments following mitochondrial stress, ubiquitination was much reduced with delayed PINK1 and DRP1 activation, which might be the result of impaired mitophagy initiation.67 In a fly HD model, over-expression of PINK1 corrected mitophagy and improved mitochondrial health.9 This suggests that the expression of high levels of HTT fragments itself promoted the induction of mitochondrial fission and resulted in slower, less dynamic mitophagy in response to stress. The gene discussed is PINK1; the disease is Huntington disease.