However, since MYC remains activated throughout Vκ*MYC progression, the subsequent decrease in ISR-GCN2 activity in int-MM mice (Fig. 4c) and the subclonal nature of ISR-GCN2 activation in active-MM mice (Fig. 4a) suggests that GCN2 activation may be regulated by other mechanisms that drive amino acid deficiency. Here, EIF2AK4 is linked to Miyoshi myopathy.