More importantly, CLDN4-enhanced cell proliferation, migration, and tumor growth, as well as intracellular levels of cholesterol and triglyceride, were prevented in T47D:dKO:CLDN4:LXRβS432A cells compared with that in T47D:dKO:CLDN4:LXRβ cells, indicating that LXRβS432 is responsible for the CLDN4/SFK/AKT-accelerated breast cancer metabolism and progression. This evidence concerns the gene NR1H2 and breast carcinoma.