However, p27S10A was not completely refractory to the toxic effect of the chemotherapeutic agents (Figure 6e), which could be attributed to the fact that the S10A forms of p27 were efficiently ubiquitylated when RBX1 was present but the p27T187A mutant was not.8,9 Thus, our data indicated that the reduction of RBX1 could represent a predominant mechanism wherein cell-cycle progression is inhibited in adherent myeloma cells via p27 up-regulation. This evidence concerns the gene RBX1 and plasma cell myeloma.