We speculated that LGALS1 acted as a co-activator of PPARγ after entering the nucleus, directly enhancing its transcriptional activity, thereby up-regulating FASN, ACC and other fat-synthesis genes; or up-regulating CD36 expression, accelerating the cell uptake of circulating free fatty acids, and then inducing T-cell exhaustion through lipid enrichment to accelerate tumor metastasis. This evidence concerns the gene PPARG and neoplasm.