STAT3 has been shown to promote tumor initiation of different tumor types, including those of the gastrointestinal tract and skin (reviewed in refs 30, 31,32), and PTK6 was previously shown to promote STAT3 activation and tumorigenesis in mouse models of colon and skin cancer.19,22 We show that mammary tumor latency is increased in Ptk6−/− MMTV-ERBB2 mice (Figure 1), and our studies suggest that PTK6-mediated regulation of STAT3 activation promotes ERBB2-induced mammary gland tumor initiation. The gene discussed is PTK6; the disease is neoplasm.