Mechanistically, circPLIN2 not only increased the stability of the c-Myc and MARCKSL1 mRNAs by binding to the KH domains of IGF2BP proteins but also competitively sponged miR-199a-3p to abolish the repressive effect of miR-199a-3p on ZEB1 expression, ultimately resulting in ccRCC tumorigenesis and progression. The gene discussed is MARCKSL1; the disease is nonpapillary renal cell carcinoma.