Studies have shown that circMYLK produced by human myosin light chain kinase (MYLK) can competitively bind to miR-29a, abolishing miR-29a inhibition of VEGFA/VEGFR2 and downstream Ras/ERK signaling pathways, thereby promoting epithelial-mesenchymal transition and bladder cancer development (Zhong et al. 2017). The gene discussed is MYLK; the disease is urinary bladder cancer.