Inflammatory breast cancer (IBC) is an aggressive subtype of breast cancer with dismal patient prognosis. Although by some considered to be just a tumor type at the extreme side of the breast cancer spectrum, there is compelling evidence to regard IBC as a distinct clinical subtype. First, IBC can be distinguished based on its unique clinical presentation with suddenly occurring and quickly escalating signs of inflammation that affect the breast. For this reason, IBC is assigned to a separate category in the TNM classification system. Second, IBC cells have an exceptional metastatic potential across all molecular subtypes, resulting in lymph node metastases being observed at time of diagnosis in all patients. Third, studies suggest that IBC exhibits an altered therapeutic response profile. For example, estrogen receptor (ER) positive disease in IBC is not associated with favorable prognosis (Liu et al., 2017), which may be due to altered ER signal transduction pathways caused by or resulting in the overrepresentation of the luminal B phenotype in ER+ IBC (Van Laere et al., 2013). Along the same lines, genes overexpressed in ER+ IBC relative to ER+ non-IBC (nIBC) are predictive of resistance to hormonal therapy (Jansen et al., 2015). When considering anti-HER2 treatment, large retrospective analyses demonstrated that the ERBB2 expression level or the ERBB2/CEP17 ratio has limited predictive and prognostic power (Kogawa et al., 2020, Masuda et al., 2014, Tarantino et al., 2022). Fourth, IBC presents with florid lymphovascular tumor emboli and a distinctive growth pattern (Vermeulen et al., 2009). Finally, biological and molecular differences between IBC and nIBC cells (e.g. higher levels of cell proliferation, RhoC and E-Cadherin overexpression, loss of WISP3 expression) have long been recognized (Lim et al., 2018).