This finding is further supported by studies using cellular models of AD: exposure of neurons to oligomeric Aβ42 increases ROCK1 and ROCK2 expression and induces phosphorylation of Lim Kinase 1 (LIMK) downstream of RhoA, while depletion of ROCK1 reduces toxic Aβ42 production (Henderson et al., 2016). The gene discussed is ROCK1; the disease is Alzheimer disease.