Although these results identify a central role for FABP5 for cancer cell proliferation and might explain the differences observed regarding PPARβ/δ and cancer cell proliferation dependent on the presence/absence of FABP5 and amounts of RA and endogenous PPAR ligands, the situation for in vivo experimental and clinical studies might be even more complex due to the interplay of the different hallmark capabilities. The gene discussed is PPARD; the disease is cancer.