Tumour cells can harbour invadopodia (actin-rich protrusions that degrade extracellular matrix components to drive cell invasion). Artym et al. devised a new system for studying invadopodia formation, which is based on high-density fibrillar collagen (HDFC) and mimics in vivo cancer environments, and found that HDFC induces the formation of ECM-degrading invadopodia in tumour cells. Mechanistically, α2β1 integrin was required for HDFC-induced invadopodia formation in breast carcinoma cells although, surprisingly, no changes in gene or protein expression were observed. However, the formation of HDFC-induced invadopodia required a different integrin signalling network to that of invadopodia induced by gelatin (an established system for studying them). Notably, phosphorylation of the integrin activator kindlin 2 as well as downstream signalling were crucial for the formation of invadopodia in cells grown on HDFC but not gelatin. Thus, HDFC activates kindlin 2 to induce invadopodia formation.