It was further shown that a serine threonine proline-rich (STP) segment of the GPR56-NTF mediated its interaction with TG2 specifically and deletion of the STP segment lead to GPR56 activation via a protein kinase C (PKC) α-dependent pathway to promote VEGF production and tumor angiogenesis [32]. The gene discussed is ADGRG1; the disease is neoplasm.