However, although knockout models are unquestionably indispensable instruments for establishing the neurobiological bases of depression, and maLPA1-null mice represent a good animal model of anxious depression, the constitutive lack of one target gene in general, or the LPA1 receptor gene (Lpar1) in particular, can induce compensatory mechanisms throughout the lifespan of the organism, causing several developmental neuroadaptations that might result in the observed deficits (El-Brolosy and Stainier, 2017). The gene discussed is LPAR1; the disease is major depressive disorder.