conditionally deleted Lats1 and Lats2 (Lats1/2) in CFs and used single-cell sequencing to show that Lats1/2 deletion led to an ongoing CF-derived proinflammatory cascade that promoted myeloid cell influx, activation, and expansion in sham hearts and post-MI hearts (94). The gene discussed is LATS1; the disease is myocardial infarction.