After lapatinib treatment, HER2, AKT, and ERK1/2 protein phosphorylation levels were undetectable in all cell lines, but baseline phosphorylation of p65 and IκB was maintained (Fig. 4c, S5B and C), demonstrating that NF-κB activation is not dependent on ErbB signaling and may support the survival of HER2-positive breast cancer cells in the presence of lapatinib. The gene discussed is NFKB1; the disease is breast cancer.