Rab1B is observed to be aberrantly down-regulated in triple-negative breast cancer (TNBC), and Rab1B deficiency stimulates the proliferation and migration of TNBC cells by diminishing degradation of ubiquitin, elevating phosphorylation levels of SMAD3 and up-regulating TGF-β-triggered EMT (Jiang et al. 2015), which increases the expression of TGF-β receptor 1 (TβR1). This evidence concerns the gene RAB1B and triple-negative breast carcinoma.