FLP enables the formation of cell-ECM adhesion plaques which then promotes dormancy-to-proliferation switch of BCC through activation of a FAK-Src-ERK signalling axis.6,7 Consistent with our outgrowth data, stable KD of Pfn1 significantly inhibited the FLP-forming ability of MDA-231 cells in MoT culture, as judged by the relative % of FLP-positive cells in control (~55%) vs Pfn1-KD (~10%) groups (Fig. 3a and supplementary Fig S5A). The gene discussed is PTK2; the disease is skin basal cell carcinoma.