Our primary aim of this study is to elucidate the potential involvement of KCa3.1 and LRRC8A in regulating CCL2 expression and production through these signaling axes in M2-MACs, as well as their role in CCL2 upregulation under high-[K+]e conditions that mimic the tumor microenvironment. This evidence concerns the gene LRRC8A and neoplasm.