Rolf Ohlsson, group leader of the mammalian epigenetics lab at Sweden's Uppsala University, wrote in an accompanying editorial that the findings may cause a shift in perspective on how scientists view illnesses believed to have a genetic component. "Anyone unfortunate enough to possess the 'wrong' set of monoallelically expressed genes might be susceptible to the earlier onset of a complex disease, such as Alzheimer's," his commentary read. "Considering the interplay among genotype, epigenotype and gene inactivation [these findings] will become more important in understanding developmental mechanisms and the penetrance of diseases in an individual as well as responses to medical treatments."

Next up: Chess says his lab will try to find triggers for monoallelic expression and probe whether genes can produce protein from one or both alleles at different times throughout a person's life span.

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