The selective knockout of β3 integrin in pericytes has been shown to promote tumor growth via focal adhesion molecule (FAK)-Akt-NF-kβ activation toward the secretion of paracrine factors such as CXCL1, TIMP-1, and CCL2, which mediate cancer proliferation toward the MEK1-ERK1/2-ROCK2 axis without interfering with blood vessel density, perfusion, or tumor hypoxia (Wong et al., 2020). The gene discussed is NFKB1; the disease is neoplasm.