Rationale: Leiomyomatosis peritonealis disseminata (LPD) is a rare benign lesion primarily consisting of smooth muscle cells, which mostly affects premenopausal females. Here, we reported 3 females with LPD (age, 40–48 years) admitted for pelvic masses. Patient concerns: All 3 LPD cases received laparoscopic uterine fibroid morcellation at 3, 8, and 14 years ago, respectively. Two cases were admitted for pelvic masses. One case was admitted for recurrent fibroids with pollakiuria. Diagnoses: LPD was considered in 2 cases preoperation according to imaging examination, and one of them received ultrasound-guided biopsy of the lesion in the right lobe of the liver. One case was considered as recurrent fibroids preoperation. After surgery, all cases were pathologically diagnosed as LPD consisting of benign smooth muscle cells. Interventions: A total abdominal hysterectomy, salpingo-oophorectomy, and debulking was performed for all 3 cases. Intraoperative exploration revealed that the fibroids distributed in the mesentery (3 cases), broad ligament (1 case), omentum (1 case), liver (1 case), and rectus abdominis (1 case). Outcomes: No recurrence was found during postoperative following-up (5–12 months). Lesions: Preoperative diagnosis of LPD is presented as a challenge due to unspecific clinical manifestations. Its diagnosis mainly depends on histopathologic evaluation. Surgery still is the primary treatment for LPD. For patients without reproductive desire, total abdominal hysterectomy, salpingo-oophorectomy, and debulking can be performed, and the affected tissue should be removed as much as possible based on the risk assessment.

N-methyl-D-aspartate receptors (NMDARs) are essential for excitatory neurotransmission and synaptic plasticity. GluN2A and GluN2B, two predominant Glu2N subunits of NMDARs in the hippocampus and the cortex, display distinct clustered distribution patterns and mobility at synaptic and extrasynaptic sites. However, how GluN2A clusters are specifically organized and stabilized remains poorly understood. Here, we found that the previously reported GluN2A-specific binding partner Rabphilin-3A (Rph3A) has the ability to undergo phase separation, which relies on arginine residues in its N-terminal domain. Rph3A phase separation promotes GluN2A clustering by binding GluN2A’s C-terminal domain. A complex formed by Rph3A, GluN2A, and the scaffolding protein PSD95 promoted Rph3A phase separation. Disrupting Rph3A’s phase separation suppressed the synaptic and extrasynaptic surface clustering, synaptic localization, stability, and synaptic response of GluN2A in hippocampal neurons. Together, our results reveal the critical role of Rph3A phase separation in determining the organization and stability of GluN2A in the neuronal surface.