Single-cell data linked RRAS to M1-macrophage state transitions; dual immunofluorescence showed RRAS upregulation coinciding with enhanced iNOS/LC3 co-localization (PAH R = 0.63 vs. control R = 0.12), implying RRAS-driven mitophagy modulation via inflammation. Here, MAP1LC3A is linked to pulmonary arterial hypertension.