Are the receptor tyrosine kinase (RTK) and JAK-STAT-driven proliferation pathways ‘parallel’ or ‘redundant’? And what about those of K-Ras4B versus N-Ras? ‘Parallel’ proliferation pathways accomplish a similar drug resistance outcome. Thus, are they ‘redundant’? In this paper, it is argued that there is a fundamental distinction between ‘parallel’ and ‘redundant’. Cellular proliferation pathways are influenced by the genome sequence, 3D organization and chromatin accessibility, and determined by protein availability prior to cancer emergence. In the opinion presented, if they operate the same downstream protein families, they are redundant; if evolutionary-independent, they are parallel. Thus, RTK and JAK-STAT-driven proliferation pathways are parallel; those of Ras isoforms are redundant. Our Precision Medicine Call to map cancer proliferation pathways is vastly important since it can expedite effective therapeutics.

受体酪氨酸激酶（RTK）和JAK-STAT驱动的增殖途径是“平行”还是“冗余”？那么K-Ras4B与N-Ras的对比呢？“平行”增殖途径实现了相似的耐药性结果。因此，它们是否“冗余”？本文认为“并行”和“冗余”之间存在根本区别。细胞增殖途径受基因组序列，3D组织和染色质可及性的影响，并由癌症出现前的蛋白质可利用性决定。提出的意见认为，如果它们操作相同的下游蛋白家族，则它们是多余的。如果与进化无关，则它们是平行的。因此，RTK和JAK-STAT驱动的增殖途径是平行的。Ras亚型的那些是多余的。