Additionally, our findings demonstrating that CRISPR-edited knock-in of mtNPM1 led to increased protein levels of HOXA9, MEIS1 and c-Myc, associated with increased in vitro sensitivity and in vivo efficacy to treatment with MI further explains its mechanistic linkage to the presence of mtNPM1. The gene discussed is HOXA9; the disease is myocardial infarction.