Moreover, remodeling of Ca2+ influx pathways was found to associate with cancer cell proliferation and migration.9 TRPV4 channelopathies are linked to skeletal dysplasias.12 TRPV4 has been implicated as a potential target in angiogenesis.13, 14 Activation of TRPV4 promoted the migration of breast cancer-derived endothelial cells but not endothelial cells derived from normal breast cells and TRPV4 silencing reduced arachidonic acid-stimulated migration of breast cancer-derived endothelial cells. The gene discussed is TRPV4; the disease is skeletal dysplasia.