Regarding RhoC, Hoeppner illustrated that RhoC could stimulate the proliferation of HUVECs by stabilizing nuclear β-catenin, which promotes the transcription of cyclin D1 and subsequently drives cell cycle progression [36]; In one analysis of cDNA microarrays of HCC, Okabe found that RhoC was differentially expressed in hepatitis B virus-positive HCC patients and in hepatitis C virus-positive HCC patients [37], and it modulated the cancer-related function relying on the N terminus of MDIA1 [38]. Here, CCND1 is linked to cancer.