At the tissue scale, apply spatial transcriptomics/proteomics and single-cell multi-omics to hearts and tumors from models with cell-type–specific F2RL1 deletion (cardiomyocyte, fibroblast, myeloid, tumor cell) to resolve context-specific roles, explicitly addressing the MI paradox wherein PAR-2 may be adaptive acutely. The gene discussed is F2RL1; the disease is neoplasm.