Consistently, the enhanced interaction of RAB11 with EGFR was found in the absence of BCAP31 as detected by a co-IP assay (Figure 6I), suggesting a role for endogenous BCAP31 in the inhibition of the physical RAB11-EGFR complex to facilitate the return of these receptors to the cell surface and therefore drive EGFR downstream signalling and tumour development. Here, RAB11A is linked to neoplasm.