In agreement with the positive correlation observed in the Hanamura MM Dataset, our data indicate that reduced levels of MEIS2 in wt-SKO-007(J3) cells obtained by transient transduction of validated shRNA sequences, significantly repressed mRNA expression of Cyclin E/CCNE1 in these cells (Fig. 3b) and, importantly, increased the induction of apoptosis in the presence of Seliciclib/Roscovitine (Fig. 3c), suggesting that combined inhibition of specific CDKs and targeting of MEIS2 could represent an interesting therapeutic strategy in MM. Here, MEIS2 is linked to Miyoshi myopathy.