We show that the fundamental addiction of melanoma cells to TGFβ is: induced by the presence of mutant BRAF; mediated by a SMAD4-independent pathway; and correlates with TGFβ regulation of RHOA activity, thus providing support for the notion that non-canonical signalling pathways are key mediators of pro-tumourigenic TGFβ function in melanoma. Here, SMAD4 is linked to melanoma.