Evidence of ERK1/2 as a downstream effector of FGL2 signalling has been demonstrated in a range of studies, including in FGL2-induced ERK1/2-dependent autophagy in carcinoma cell lines [59], and the silencing of FGL2 as a target of interest in tumour development has been found to be associated with a decrease in ERK1/2 phosphorylation [60]. This evidence concerns the gene MAPK3 and neoplasm.