The overexpression of circ-IARS significantly down-regulated the levels of miR-122 and ZO-1, upregulated the levels of RhoA and RhoA-GTP, increased the expression and adhesion of F-actin, enhanced the permeability of endothelium, and promoted tumor invasion and metastasis.64 Moreover, The upregulation of circ-DLEU2 promoted the expression of PRKACB by inhibiting the expression of miR-496, which promoted the proliferation of leukemia cells in vitro, blocked cell apoptosis, and promoted the formation of acute myeloid leukemia tumors in vivo.65 Here, RHOA is linked to neoplasm.