TLR4 and myelodysplastic syndrome: In this context, MACROH2A1 (MH2A1.1), a histone variant regulating epigenetic and MSC inflammation interaction in MDS, exhibited that its accumulation in MDS‐MSCs prompted pro‐tumoral TLR4 activation, ensuing in pro‐inflammatory mediator production and regulation that could impair the hematopoietic system's ability to support diseased cells [54].