Although this may follow the mechanisms previously described, as TRAF6 is an important downstream mediator of MYD88 signaling, previous studies have shown that the loss of TIFAB, a gene associated with MDS‐del5q, results in increased TRAF6 levels and altered myeloid differentiation, including neutrophil dysplasia and cytopenia [3, 51]. The gene discussed is TRAF6; the disease is myelodysplastic syndrome.