CX3CL1 and Axenfeld-Rieger syndrome: Notably, MST4 overexpression can directly inhibit CX3CL1 release through a MST4-NF-κB-CX3CL1 signaling pathway that mediates neuron–microglia interactions in the early stage of acute stress to increase microglial activation and engulfment of GABACeA neuronal spines, consequently inhibiting GABACeA neuronal activity in ARS mice.