Together, these findings indicated the oncogenic function of circPLIN2 and its potential molecular mechanism in which elevated circPLIN2 participated in the development and progression of ccRCC by binding IGF2BP proteins and miR-199a-3p to regulate the expression of their target genes, including c-Myc, MARCKSL1, and ZEB1 (Fig. 8G). This evidence concerns the gene MARCKSL1 and nonpapillary renal cell carcinoma.