In addition, Drp1 pharmacologic inhibition by mdivi-1 led to a shift from mitochondrial fission towards fusion, followed by a reduction in invasion of RACGAP1-overexpressing breast cancer cells compared to the control; notably, treatment with M1, a promoter of mitochondrial fusion, led to the same phenotypic effects, suggesting that overexpression of RACGAP1P promoted mitochondrial fission, which is necessary for the invasion of breast cancer cells [75]. Here, RACGAP1P1 is linked to breast cancer.