FBXO6 targets activated CHK1 for degradation57 and over-expression of CHK1 has been shown to contribute to HDACi resistance.58 Therefore, one could postulate that the absence of FBXO6 with subsequent impaired clearance of activated CHK1 and resulting inhibition of apoptosis may identify MM tumors where CHK1 inhibitors could be successfully combined with HDACi. Here, FBXO6 is linked to Miyoshi myopathy.