Nonetheless, the overexpression of Mcl-1 exacerbated lpr autoimmune phenotypes and accelerated the morbidity with excessive weight loss, breathing difficulties and severe lymphadenopathy in the Faslpr/lpr mouse model (non-functional Fas death receptor) (Cohen and Eisenberg, 1991; Anstee et al., 2017). The gene discussed is MCL1; the disease is Lymphadenopathy.