Recent studies reported that treatment with tamoxifen enhances neutrophil activity by increasing the neutrophil extracellular traps (NETosis) and induces changes in macrophages by inhibiting the expression of CD36 and PPARγ, thereby reducing atherosclerosis [26,27], but there are no data regarding the immune function of both cells treated with tamoxifen after a bacterial infection. The gene discussed is PPARG; the disease is atherosclerosis.