The rapid induction of apoptosis by ATX-101 could be explained by an inhibition of the binding between cytosolic PCNA and procaspases leading to direct caspase activation, similar to what was found in neutrophils by Witko-Sarsat et al.[8]; however, ATX-101 did not induce apoptosis in normal lymphocytes, monocytes, or BMSC, although monocytes showed similar cytosolic PCNA levels as MM cell lines (unpublished data). Here, PCNA is linked to Miyoshi myopathy.