With this in mind, it is notable that inhibiting the interaction of fibrinogen with CD11b is sufficient to mitigate neuroinflammatory processes and ameliorate motor function in MS while preserving its essential procoagulant functions.132,143 It is also worth mentioning that its derivative, fibrin, appears to play an important part in the cascade: the interaction of fibrin with CD11b-CD18 was shown to be necessary to induce microglia-mediated neurotoxicity in AD and MS mouse models.143. Here, ITGAM is linked to myeloid sarcoma.