Hsa-miR-26a-5p regulated six genes including the one coding for Complement C3 (C3), whose upregulation has been reported facilitating the deposit clearance80, and that coding for the Heat shock 70 kDa protein (HSPA8), which was one of the proteins demonstrated to lose their solubility following an extracellular accumulation of amyloid in a mouse model of Alzheimer-type amyloidosis81. This evidence concerns the gene C3 and amyloidosis.