ASAP1 and neoplasm: Additionally, the ARF6-AMAP1 pathway was also found to be involved in acidosis and fibrosis of the TME, both of which are well known to be barriers against immune attack to cancer cells (81, 303), indicating that the ARF6-AMAP1 pathway may also be a valuable target in modifying the TME from pro-tumor, which makes PDAC resistant to treatment, towards an anti-tumor state.