Our findings, together with the recent discovery that the actin cytoskeleton controls LPAR1 trafficking in response to self-generated gradient of LPA to sustain directional migration of pancreatic cancer cells (42), supports the general idea that the Gβγ–ARHGEF17 signaling complex might drive polymerization of the actin cytoskeleton as a signaling circuit to control lung cancer cell migration and invasion. This evidence concerns the gene LPAR1 and familial pancreatic carcinoma.