DNER and lymphoma: Albeit part of the antitumor activity of LRRK2‐IN‐1 might be due to its binding to proliferating cell nuclear antigen or to the recently discovered affinity to BET proteins in addition to LRRK2 [52, 53], we showed that both the genetic and pharmacologic silencing of LRRK2 was toxic for lymphoma cells and gives an advantage to BET inhibitors.