Activation of SRC via ectopic expression or mutation, as seen in many cancers, can suppress Rho activation and increase the formation of podosomes, which are F-actin rich structures on the cells, and cell invasion [68,69] Activation of the ERK5-MEF2c axis, but not ERK1/2, was mainly responsible for in v-SRC-transformed NIH-3T3 cells via induction of deleted in liver cancer 1 (DLC-1) expression, a negative regulator of Rho [69]. Here, SRC is linked to cancer.