CCL3+ pro-inflammatory macrophages strongly interact with fibroblasts via NLRP3, and pharmacological inhibition of CCL3+ pro-inflammatory macrophages significantly alleviated RV dilatation and dysfunction in a mouse model of ARVC.444 In addition, a single-nucleus RNA sequencing study predicted that downregulation of runt-related transcription factor 1 (RUNX1) transcriptional activity in cardiac macrophages and fibroblasts may promote cardiac recovery in patients with HF by gene regulatory network construction. The gene discussed is CCL3; the disease is Arrhythmogenic right ventricular dysplasia.