Because cAMP promotes neuronal survival (Li et al., 2000) and suppresses Parkinson’s disease (Muda et al., 2014) and tumor formation (Bierie and Moses, 2006), future studies that enable segregation of multiple function of TRIP-BR1 must further investigate how and to what extent the regulatory function of TRIP-Br1 in AC-cAMP signaling, in addition to its transcriptional function, contributes to neuronal and other deficiencies. The gene discussed is CXCL11; the disease is Parkinson disease.