ITGA6 and neoplasm: In addition, we provide evidence that SEMA7A expressing cells upregulate drug-resistant cell-surface markers [24] and therefore may not respond to conventional chemotherapy; this, along with our analysis of RFS in a large patient dataset revealing that co-expression of ITGA6 and SEMA7A significantly influences the probability of relapse suggests that SEMA7A can not only initiate tumor formation, but also influence clinical outcomes.