CXCL12 and WHIM syndrome: The enhanced and prolonged CXCL12 responses featured in WHIM syndrome (i.e., ERK1/2 signalling and chemotaxis) may also result from aberrant activation of arrestin-dependent pathways, as originally revealed by the impaired migration of leukocytes from β-arrestin 2 knockout mice in response to CXCL12 [22] and further supported by the seemingly paradoxical strengthened CXCL12-induced chemotaxis by β-arrestin 2-dependent signalling in human cells [65,66].