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. Here, DGAT1 is linked to cancer.