Although the role of NCLX in cancer is less explored than other members of the mitochondrial Ca2+ transportome, it has been shown that genetic loss of NCLX in colorectal cell lines (HCT116 and DLD1) could cause mitochondrial Ca2+ overload and inhibits proliferation and increases migration and chemoresistance by transcriptional reprogramming. This evidence concerns the gene SLC8B1 and medical procedure.