In summary, our results show that i) the ability of meprins to cleave the cancer-associated CD99 variants is not largely impaired although the cleavage site shifted, ii) both, D92H and D92Y seem to be partially misfolded and are more prone to proteasomal degradation than CD99 WT, and iii) D92H causes significantly higher cell migration compared to CD99 WT. This evidence concerns the gene CD99 and cancer.