Kamizono et al. (2001) pointed out that SOCS1 promotes ubiquitin-dependent degradation of the leukemia-associated TEL-JAK2 fusion protein. In anemia of inflammation (AI), AMPK activation induces SOCS1-mediated JAK2 degradation to relieve AI (Wang et al., 2017). However, there are few reports about SOCS1 mediating protein ubiquitination during virus infection. Du et al. (2020) found that IAV infection induces SOCS1 expression to promote JAK1 ubiquitination, which in turn inhibits host innate immune responses. Here, JAK2 is linked to anemia (phenotype).