Because it is known that Acc2 deletion increases FAO and suppresses glucose utilization in the context of LV pressure overload Matsuura et al., 2020; Ritterhoff et al., 2020, it is important to recall that cardiac myocytes within TGAC8 LV are smaller in size, and not enlarged as those in pathologic cardiac hypertrophy in response to LV pressure overload, Dorn et al., 2003 and in which ACC2 promotes glucose utilization and reduces FAO (Matsuura et al., 2020; Ritterhoff et al., 2020). This evidence concerns the gene ACACB and cardiac hypertrophy.