In light of our observations that: (i) cytoplasmic CRABP1 in breast tumors is an adverse factor in clinical outcomes and (ii) CRABP1 accumulates in the cytoplasm of cells treated with RA, we propose that the primary role of CRABP1 in breast cancer is to sequester RA in the cytoplasm, thereby preventing RAR activation in the nucleus (Fig. 6b). This evidence concerns the gene CRABP1 and breast carcinoma.