This outcome was possibly due to increased levels of apoptosis and inflammation.74 Similarly, deletion of JNK1, JNK2, or JNK3 did not affect pressure overload-induced cardiac hypertrophy, but JNK1 deletion led to the rapid deterioration of cardiac function, which was associated with increased apoptosis and inflammatory infiltration in the heart.75 Another study indicated that JNK was a negative regulator of cardiac hypertrophy. This evidence concerns the gene MAPK9 and cardiac hypertrophy.