Interestingly, the tyrosine phosphatase, SHP2, that has been demonstrated to increase expression of ACSL4 protein in MA-10 Leydig cells [77], has been shown to promote breast cancer progression [78] and to increase motility of TNBC [79], while inhibition of SHP2 induces a basal-to-luminal transition in breast cancer cells characterized by ER expression, estrogen growth dependency and sensitivity to anti-estrogen therapy [80]. This evidence concerns the gene ACSL4 and breast carcinoma.