Guttikonda et al. (2021) reported that astrocytes secrete high levels of C3 upon LPS stimulation in the triple AD co-culture derived from human PSC. LPS might induced stronger inflammatory response than 3 μM oligomeric Aβ, but interestingly our results are complementary to those ones, since we report high levels of CD11b, one of the subunits of the CR3, receptor for cleavage products of C3. Both microglia and astrocytes can participate in synaptic elimination via the complement system (Hong et al., 2016) and MEGF10/MERTK pathways (Chung et al., 2013), respectively. The gene discussed is C3; the disease is Alzheimer disease.