CD36 and cancer: Interestingly, the PKC-ζ pseudo-substrate inhibitor (that prevented CD36 translocation) also blocked DGAT1 upregulation in 6.5/cancer cells (Fig. 4n and Supplementary Fig. 4l) and in TGF-β2-treated cancer cells (Supplementary Fig. 4l, m), suggesting that CD36 cell surface expression could be the primary event leading to subsequent upregulation of genes involved in FA handling.