Furthermore, the exogenous up-regulation of TRPV4 in breast cancer has been shown to aid actin dynamics and lead to higher activation of cofilin, a downstream protein effector of RhoA/ROCK pathways that promotes actin filaments depolymerisation, thus conferring cellular “softness” and promoting transendothelial migration (Lee et al., 2016). The gene discussed is TRPV4; the disease is breast carcinoma.