Moreover, the ERK1/2 inhibition also blocked p38 activation, indicating that ERK1/2 acts at the upstream of p38 and BMSC-exosomes regulate VEGF expression through ERK1/2-p38 MAPK pathways, resulting in enhanced tumor angiogenesis which in turn promotes the tumor growth in vivo [17]. The gene discussed is MAPK3; the disease is neoplasm.