The expression of p27 is mainly regulated by proteasomal degradation mediated by the SCF‐ ubiquitin ligase complex, which includes Skp2 for specific recognition of p27 as a substrate.41, 50 In our previous studies in glioblastoma cells, p27 accumulation following depletion of 14‐3‐3ζ or β was attributable to the decrease in Skp2 mRNA through the loss of STAT3 or ERK activity following 14‐3‐3ζ or β depletion, respectively.28, 29 However, the increase in Skp2 protein levels was not the primary cause of p27 accumulation in the present study (Figure 3E,F). Here, STAT3 is linked to glioblastoma.