CD4 and pancreatic neoplasm: This suggests that EGFR, SERPINB5, MYEOV, GPRC5A, and KRAS may drive further pancreatic cancer development by recruiting pro-tumor-associated immune cells such as monocytes, nTreg cells, and Th17 cells through downstream responses while inhibiting the infiltration of tumor-suppressive immune cells such as CD4 T cells, γδT cells, MAIT cells, NK cells, Tfh cells, and CD8T cells to reduce tumor-associated immune killing [19,20,21,22].