Although we cannot exclude a contribution from this process, there are three lines of evidence to suggest that the majority of effects we describe are due to NMDAR–BK coupling: 1) NMDAR activation resulted only in BK channel–mediated current, 2) BK-specific inhibition completely abolished the t-LTP differences between A-type and B-type BC-L5PNs, and 3) BK-mediated inhibition of NMDARs remained when basal afferent inputs were electrically stimulated and was independent of back-propagating action potentials. This evidence concerns the gene KCNMA1 and breast cancer.