We have also reported that bi-allelic deletion of FAM46C by the CRISPR-Cas9 system enhances cell proliferation along with activation of PI3K-Akt signaling, and the Akt inhibitor afuresertib is more effective in suppressing cell growth in MM cells with disrupted FAM46C than in parent cells with wild-type (WT) FAM46C [84]. Here, AKT1 is linked to Miyoshi myopathy.