In this regard, the genomic landscape of acute myeloid leukemias is known to show frequent alteration of components of RAS pathways [45], where SOS1 is a recognized key regulator of downstream signaling initiated not only by normal, non-mutated RAS cellular proteins but also by ontogenically mutated, cancer-inducing RAS isoforms [18,46]. The gene discussed is SOS1; the disease is cancer.