Remarkably, this revealed that, despite the relatively low r2 for each individual chemokine, a highly significant (p = 0.0008), four-chemokine model including CCL17 (TARC), CCL11 (Eotaxin), CCL2 (MCP-1), and PDGF-BB could explain about 80% of the variation in the proportion of HMC/CD34 in our cohort of SCD and healthy individuals (Figure 4B). The gene discussed is CCL11; the disease is Schnyder corneal dystrophy.