Combined, this suggests a model where a well-established multitude of interactions between MTs and contracting peripheral F-actin stress-fibers (via conventionally known MT–actomyosin interactions adaptors, such as myosin, and TIP50 and septin49 complex, which can be overexpressed in some carcinoma cells52) are necessary to promote Arp2/3-dependent uniaxial dimensionality commitment on biaxial contact guidance cues (Fig. 6b). The gene discussed is MYH14; the disease is carcinoma.