For example, it has been reported that, similar to CX3CR1 deficiency, amyloid precursor protein/presenilin-1 (APP/PS1) mice lacking CX3CL1 showed reduced amyloid pathology, and expression of obligate sFKN in this context did not improve or exacerbate this effect [25]. This evidence concerns the gene CX3CL1 and amyloidosis.