Whereas, the teratogenicity of thalidomide-like drugs appears to be driven by cereblon-triggered degradation of SALL4 and associated transcription factors [69,83,84,112], and the classical adverse actions of clinically approved IMiDs, when used in cancer treatment (anemia, neutropenia, thrombocytopenia [149]), potentially derive from their anticancer actions mediated via cereblon triggered Ikaros/Aiolos degradation, and may or may not occur in the described new IMiDs that do not induce such degradation. This evidence concerns the gene IKZF1 and anemia (phenotype).