When ERO1α is knocked out using CRISPR Cas9 in HCT116 colorectal cancer cells and placed under hypoxic conditions it was found that the glycosylation state of integrin β1 was changed and thus an attenuation of integrin β1 on the cell membrane occurred; ultimately leading to contact-inhibited morphology [57]. The gene discussed is ERO1A; the disease is colorectal cancer.