Notably, the cytoplasmic abundant lncRNA, RC3H2, could physically interact with miR-101-3p, while suppression of miR-101-3p could attenuate the lncRNA RC3H2 knockdown-induced inhibitory effects on OSCC cells by targeting EZH2, revealing that lncRNA RC3H2 could act as ceRNA to up-regulate EZH2 expression by sponging miR-101-3p (Figure 1d), which subsequently affected the level of H3K27me3 deposition and the expression of downstream genes associated with cancer progression [53,54]. The gene discussed is EZH2; the disease is cancer.