We speculate that this discrepancy may be because of the abnormal increase in BMP4 in the AD model [59] and that abnormal activation of BMP4 may induce TFAP2B upregulation through feedback mechanisms to maintain neural microenvironment homeostasis or mitigate neuronal damage, reflecting the compensatory enhancement of TFAP2B in a pathological state. Here, BMP4 is linked to Alzheimer disease.