Omicron has more than twenty new mutations in the S1 domain of the spike gene as compared to the other previously known variants of SARS-CoV-2. Many of these new mutations, especially those located in the receptor binding domain, are likely to improve binding to the ACE2 receptor and to avoid binding to antibodies induced by a previous infection or by vaccination. Today there are several different hypotheses about the origin of Omicron, for example that it would have arisen in an immunosuppressed individual. Alternatively, a SARS-CoV-2 variant could have infected an unknown animal, and re-infection of humans would then have occurred. Furthermore, Omicron may have picked up a piece of a human common cold coronavirus. The hitherto available data suggest that the rapid spread of Omicron is a combination of properties of the virus replication ability in addition to its ability to avoid pre-existing immune responses.