The observation of ALK gene expression in TNBC in general is consistent with the present results demonstrating the prevalence of increased ALK copy number, low level gene amplification and/or ALK pathway activation in IBC pre-clinical models of triple negative IBC; This observation is also consistent with the detection of ALK abnormalities in IBC tumors and with the identification of ALK copy gains in basal-like breast cancers that have an "IBC-like" gene signature. The gene discussed is ALK; the disease is breast cancer.