We then integrate data of transcriptomic dysregulation in AD brains with the expanded AD disease module, considering the transcriptomic data from both the temporal cortex as major disease-relevant tissue, and the cerebellum as the hypothesized control, based on the evidence that tau pathology, the pathological feature of AD that closely associated with clinical symptoms, emerges in temporal cortex early in the course of the disease before spreading to the other cortical areas in later stages, with minimal involvement to the cerebellum [25–29]. The gene discussed is MAPT; the disease is Alzheimer disease.