Sporozoite forms of the malaria parasite Plasmodium are transmitted by mosquitoes and first infect the liver for an initial round of replication before parasite proliferation in the blood. The molecular mechanisms involved during sporozoite invasion of hepatocytes remain poorly understood. In previous studies, two receptors of the Hepatitis C virus (HCV), the tetraspanin CD81 and the Scavenger Receptor BI (SR-BI), were shown to play an important role during entry of Plasmodium sporozoites into hepatocytic cells. In contrast to HCV entry, which requires both CD81 and SR-BI together with additional host factors, CD81 and SR-BI operate independently during malaria liver infection, as sporozoites can use CD81 and/or SR-BI, depending on the Plasmodium species, to invade hepatocytes. However, the molecular function of CD81 and SR-BI during parasite entry remains unknown. Another HCV entry factor, the Ephrin receptor A2 (EphA2), was recently reported to play a key role as a host cell entry factor during malaria liver infection. Here, we investigated the contribution of EphA2 during CD81-dependent and SR-BI-dependent sporozoite infection. Using small interfering RNA (siRNA) and antibodies against EphA2, combined with direct detection of parasites by flow cytometry or microscopy, we show that blocking EphA2 has no significant impact on P. yoelii or P. berghei host cell infection, irrespective of the entry route. Thus, our findings argue against an important role of EphA2 during malaria liver infection.