Adipocytes are the specialized cells for lipids storage and form the major cellular component of the breast organ microenvironment. The adipose tissue next to the breast tumor consists of modified adipocytes that share similarities with their precursors, known as pre-adipocytes. Understanding the interaction between both cell types will guide novel therapeutic strategies to treat breast tumors. Here, we identify RET receptor tyrosine kinase as a breast tumor-adipose tissue interplay regulator. RET is overexpressed in 40% of breast tumors and high RET correlates with decreased survival in patients. RET-expressing tumors in our in vivo mouse models display abnormal adjacent adipose tissue. RNA-sequencing analysis revealed significant upregulation of genes involved in maintaining a pre-adipocyte phenotype, such as PDGF ligands, in RET-expressing glands compared to controls. Accordingly, in human breast tumor biopsies RET expression positively correlates with PDGFB. Mechanistically, we first have confirmed in vitro that PDGFB acts as a tumoral RET signaling downstream factor. Then, using co-culture systems of adipocyte cultures with RET-WT or CRISPR/Cas9-edited RET-KO tumor cells we pinpoint the effects of RET to keep PDGFR-positive pre-adipocytes phenotype. We show that the loss of RET on tumor cells reestablishes the adipocyte differentiation process. For that, we measured lipid incorporation and specific markers of adipocyte maturity. Importantly, we demonstrate that pre-adipocyte cells act as pro-tumoral in a RET-dependent manner. We found that co-cultures with pre-adipocytes enhance the proliferation of RET-WT cells. Furthermore, in vivo co-injection of pre-adipocytes and breast cancer cells promotes tumor growth in RET-WT tumors. Thus, the tumoral RET/PDGFB axis drives the harmful contribution of adipose tissue to breast cancer progression.