Zhang et al. (2019) has carried out a trial in a mouse model of AD and reported that FPR2 deficiency facilitated activation of astrocytes and prognosis improvement. A previous U87 astrocytoma cell model study showed that the stimulation of FPR2 in vitro increased MAPK activities, which could be abrogated in the presence of an FPR2 antagonist. FPR2-induced ERK and JNK augment the expression of glial fibrillary acidic protein and IL-1α, which are correlated with reactive astrocytosis (Kam et al., 2007). This evidence concerns the gene FPR2 and astrocytoma (excluding glioblastoma).