Based on the signaling cascades and mechanisms observed in cancer (described above), the increased level of FABP7 in AD brains, and the evidence for AA-mediated AD progression and DHA-mediated neuroprotection, we hypothesize that FABP7 serves a dichotomous role in neurodegeneration, with the relative AA:DHA ratio ultimately determining FABP7’s cellular function (Figure 2) and, consequently, AD pathogenesis and progression. The gene discussed is FABP7; the disease is Alzheimer disease.