Indeed, a previous study demonstrated that QKI interacted with E2F1 in a negative feedback loop to regulate cell cycle distribution.13 Other previous studies revealed that QKI could either increase or decrease the stability of target mRNAs.13, 16, 38 In our current study, we treated bladder cancer cells after QKI‐6 knockdown or overexpression with a gene transcription inhibitor, actinomycin D, and found that QKI‐6 destabilized and reduced E2F3 mRNA and protein respectively. The gene discussed is E2F1; the disease is urinary bladder carcinoma.