Recent work suggests that BC controls AMPAR and Kv1 channel clustering on parvalbumin-positive interneurons [84], and our own preliminary data show a regulation of small-conductance Ca2+-activated K+ (SK2) channels by BC in principal cells [85], raising the possibility that proteolytic degradation may thus locally change excitability and efficacy of synapses. The gene discussed is PVALB; the disease is breast cancer.