To validate this hypothesis, we utilized a modification-specific antibody against H2Aub (K119) and demonstrated that both EnP1 overexpression (Fig 2A and 2B) and microsporidia infection (Fig 2C and 2D) significantly elevated H2Aub levels in host cells, independent of total H2A protein abundance (S2A and S2B Fig). The gene discussed is BYSL; the disease is microsporidiosis.