Wang et al. (2012) identified that the normal function of FLNA is altered in AD, detaching itself from actin filaments and enabling Aβ42 to activate neuroinflammation and tau hyperphosphorylation pathways. The same research team attributed this change of function to an alteration of the structure of FLNA caused by Aβ42, with the vast majority of FLNA found in the post-mortem AD brain being in its altered state (Burns and Wang, 2017; Wang et al., 2017). The gene discussed is MAPT; the disease is Alzheimer disease.