Because CD36, a phagocytic receptor that mediates fatty acid–induced metastasis via regulating fatty acid intake and metabolism, is selectively upregulated in the intratumoral Tregs and functions as a central metabolic modulator that fine-tunes mitochondrial fitness in LA-rich TME (16, 21–23), we then examined the expression of CD36 in the tumor-infiltrating Tregs. Here, CD36 is linked to neoplasm.