Patients with C1q deficiency develop lupus with high penetrance[39] and have high levels of IFNα in the serum and cerebrospinal fluid[40], presumably from defective clearance of apoptotic debris and lack of the inhibitory effect that C1q has on IFNα production by pDCs and monocytes[40]. Here, IFNA2 is linked to systemic lupus erythematosus.