As a completely new principle and new active substance for plant protection, unmodified DNA was shown to function as contact insecticide in 2008. CUAD (contact unmodified antisense DNA) biotechnology is built on the use of short antisense DNA oligonucleotides for insect pest control. Being a novel class of insecticides, oligonucleotide insecticides target pest rRNAs and/or pre-rRNAs and recently showed high insecticidal potential against sap-feeding insect pests, main vectors of plant DNA viruses and one of the most economically-damaging groups of herbivorous insects. In order to use all possible opportunities of CUAD biotechnology, in this article we investigated insecticidal potential of short 11-mer antisense DNA oligos in comparison with long 56-mer single-stranded and double-stranded DNA sequences for Coccus hesperidum control and found lower efficiency of the latter. Also in this article we show that DNA containment (DNAc) mechanism, found on sternorrhynchans, represents interesting and important for insect cell life interplay between rRNAs and different types of DNA oligos. In the course of DNAc, hypercompensation of target rRNA is triggered by all highly and all somewhat complementary DNA oligos but more pronounced later degradation of target rRNA and significant insect pest mortality is seen only in the case of perfect complementarity of oligonucleotides to target rRNA. Oligonucleotide insecticides are effective and safe control agents against sternorrhynchans and other groups of pests, easy to ″tune″ to particular crops with pests, and also flexible to instantly re-create new oligonucleotide insecticides in the case of target-site resistance. Minimalist approach, short antisense DNA dissolved in water, is so potent and selective eco-friendly innovation against sternorrhynchans and other pests, and reveals entirely new dimension to plant protection — DNA–programmable insect pest control. Fundamentally important, this surprising results reveal completely new principle of regulation of rRNA expression in the cell via complementary interaction between rRNAs and unmodified antisense sequences of cell and viral DNA.