Under RA inflammatory conditions, RA-FLS acquire an aggressive phenotype, such as lost contact inhibition, boosted migration and invading properties, and resisted apoptosis, and also the elevated expression of molecules that modulate inflammation, angiogenesis, extracellular matrix degradation, such as VCAM-1, ICAM-1 and cadherin-11, finally leading to synovial hyperplasia (Cao et al., 2020). The gene discussed is VCAM1; the disease is rheumatoid arthritis.