Thus, our data support the role of Kindlin-2 in both cancer cells (4T1, MDA-MB-231 [24,25], and E0771 and HML2 BC cells, present study) and the tumor microenvironment (MECs), which suggests that a potential successful treatment of BC may require a dual targeting of Kindlin-2 and/or its downstream signaling in both the tumor and the tumor microenvironment. This evidence concerns the gene FERMT2 and neoplasm.