Collectively, these analyses indicate that Cx26 expression may be uniform across breast cancer subtypes, excluding the PR-positive subtype, but that when FAK and NANOG are expressed together with Cx26, the permissive cellular environment of TNBC cells allows the formation of a Cx26/FAK/NANOG complex that may drive CSC maintenance by activating self-renewal. The gene discussed is PTK2; the disease is breast cancer.