In turn, the adipose microenvironment contributed to re-programming H295R cells toward a more invasive phenotype, by changing their metabolic requirements and dependence from the IGF2 paracrine axis to the ASC-dependent leptin production, and inducing a shift in the expression of chemokine receptors involved in supporting tumor invasion from CXCR4 to CXCR7. Here, ACKR3 is linked to neoplasm.