Moreover, this type of cytotoxicity does not appear to be associated with the overexpression of DUF1619, as the N-DUF1619 strain exhibits a higher level of N-DUF1619 but maintains a phenotype consistent with tctn1. Unlike comprehensive complementary studies of the key TZ protein CEP290, the C-terminal domain of CEP290 could effectively rescue retinal degeneration in the CEP290 mutant as a promising gene therapy strategy,41 while the expression of N-terminal CEP290 could also restore the interactor’s TZ localization and ameliorate defects in TZ initiation in the corresponding mutant.42 The gene discussed is TCTN1; the disease is retinal degeneration.