Inhibition of ER-Golgi traffic has been reported to trigger α-synuclein aggregation, suggesting that an increase in production of Rab1 proteins can potentially rescue this α-synuclein toxic phenotype.15 Further research is required to understand the role of Rab1A and Rab1B in various diseased states and their potential as therapeutic targets to slow the progression of cancer and neurodegeneration. The gene discussed is RAB1B; the disease is cancer.