AXL and viral infectious disease: For instance, the presence of PFME on the cells could downregulate expression of the host cell factors that facilitate EBOV attachment and entry (β1 integrins, folate receptor-α, C-type lectins, T-cell immunoglobulin and mucin domain 1, and Tyrosine kinase receptor Axl) [64,65,66,67,68,69,70,71,72], modulate host macropinocytosis that promotes EBOV particle engulfment [10,73], or boost the innate antiviral immune response which is known to block viral infection [74].