RhoJ is a Rho GTPase that belongs to the Cdc42 subfamily and has a molecular weight of approximately 21 kDa. It can activate the p21-activated kinase family either directly or indirectly, influencing the activity of various downstream effectors and playing a role in regulating the cytoskeleton, cell movement, and cell cycle. RhoJ's expression and activity are controlled by multiple upstream factors at different levels, including expression, subcellular localization, and activation. High RhoJ expression is generally associated with a poor prognosis for cancer patients and is mainly due to an increased number of tumor blood vessels and abnormal expression in malignant cells. RhoJ promotes tumor progression through several pathways, particularly in tumor angiogenesis and drug resistance. Clinical data also indicates that high RhoJ expression is closely linked to the pathological features of tumor malignancy. There are various cancer treatment methods that target RhoJ signaling, such as direct binding to inhibit the RhoJ effector pocket, inhibiting RhoJ expression, blocking RhoJ upstream and downstream signals, and indirectly inhibiting RhoJ's effect. RhoJ is an emerging cancer biomarker and a significant target for future cancer clinical research and drug development.