RXFP1 and glioblastoma: This increase in Cdc42 protein was critically dependent on the presence of RXFP1 and abolished upon selective siRXFP1 knockdown (KD), while basal Cdc42 protein levels in patient GBM and U87MG cells remained unchanged by RXFP1 silencing alone or in combination with CTRP8 treatment (Fig. 1A–F).