Presently, mutations across >50 distinct genes associated with complement pathways (such as C1, C2, C4), type I interferon signalling (including DNASE, RNASE, TREX, IFIH1, ADAR), mechanisms of self-tolerance (for example, PRKCD, TNFSF13B) or RAS signalling pathways (like PTPN11, SOS1, KRAS, SHOC2) are indicated in the aetiology of monogenic lupus [2]. The gene discussed is PTPN11; the disease is systemic lupus erythematosus.