Our data suggest that (i) ALK2 inhibits migration by suppressing RAC1/RAC1b protein expression, (ii) ALK2 and RAC1b act together in a negative feedback loop to mutually control their expression and signaling, and (iii) the ALK2 antimigratory function appears to be particularly crucial in protecting epithelial subtype cells from becoming invasive, both spontaneously and in a TGFβ-rich tumor microenvironment. This evidence concerns the gene ACVR1 and neoplasm.