Since STAT1 has been shown to play a pivotal role in type I and type II interferon (IFN) signaling and possess tumor suppressor activities, particularly in mammary tumor formation [66,67,68], we hypothesized that one mechanism by which SPHK1 might promote breast CSCs’ and non-CSCs’ survival is through suppression of STAT1. The gene discussed is IFNA1; the disease is neoplasm.