Further studies showed that, in stark contrast to HCC, suppressing the expression of RhoGDI2 also increased the phosphorylation of Akt and PI3K, hinting that RhoGDI2 may exert anti-tumoural activities in LUAD by decreasing Rac1 activity and deactivating the PI3K/Akt pathway [48,49]. This evidence concerns the gene ARHGDIB and hepatocellular carcinoma.