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. Here, SEMA7A is linked to neoplasm.